Baikal skullcap

Last Updated: September 28, 2022

Scutellaria baicalensis (Chinese Skullcap) is a traditional chinese medicine for the purposes of cardiovascular and cognitive health as well as longevity. It appears to be a good source for flavonoid compounds, and some components are quite potent.


Baikal skullcap is most often used for

Don't miss out on the latest research


Sources and Composition



Scutellaria baicalensis (of the Labiatae family) is a plant sometimes referred to as Huang qin or Scutellariae radix (when referring to the root) and has usage in Traditional chinese medicine (TCM) for the treatment of cardiovascular disease,[1] bleeding disorders (hematemesis, hematuria, and metrorrhagia),[2]

The related plant, Scutellaria lateriflora, is commonly referred to as Skullcap; this term is sometimes also applied to Scutellaria baicalensis along with the names 'Golden Root' (this name also applies to Rhodiola Rosea by pure chance).[3]

Scutellaria baicalensis is a component of various combination therapies (from TCM) including Ger-Gen-Chyn-Lian-Tang (rhizome of Coptidis chinensis paired with the roots of Pueraria Lobata, licorice, and scutellaria baicalensis),[4] Soshiho-tang (Bupleurum falcatum, licorice, panax ginseng, ginger, ziziphus jujuba, and Pinellia ternata with scutellaria baicanelsis),[5] and shuanghuanglian (forsythiae fruits and honeysuckle with scutellaria baicanelsis).[6]

Scutellaria baicalensis is a traditional chinese medicine used for general preventative health purposes, with a bit more focus towards cardiovascular and bleeding disorders as well as neuroprotective/cognitive enhancing properties



  • Baicalin (Baicalein-7-glucuronide)[7][8] and its aglycone baicalein, as well as another glycoside known as baicalein-7-O-glucoside[9]
  • Wogonoside (wogonin-7-glucuronide) and its aglycone Wogonin[8] as well as another glycoside known as Wogonin-5-O-glucoside[9]
  • Oroxylin A (5,7-dihydroxy-6-methoxyflavone)[10] and its 7-O-glucoside[9]
  • Neobaicalein
  • Scutellarin and Isoscutellarein[11]
  • Chrysin[12]
  • Viscidulin I and Visdulin III[12]
  • Skullcapflavone I[13] and II[12]
  • (2R,3R)-2′,3,5,6′,7-pentahydroxyflavanone[14][15]
  • (2S)-5,7,2′,6′-tetrahydroxyflavanone[12]
  • (2S)-5,7-dihydroxy-6-methoxyflavanone[12]
  • 5,7,2'-trihydroxy-6,8-dimethoxyflavone (K36)[12]
  • 6,2′-dihydroxy-5,7,8,6′-tetramethoxyflavone[12]
  • 5,7,4′-trihydroxy-8-methoxyflavone [12]
  • Apigenin (as 6-C-glucoside 8-C-arabinoside)[11]
  • Luteolin and 6-hydroxyluteolin[11]
  • Carthamidin (as 7-O-glucuronic acid) and Isocarthamidin-7-O-glucuronic acid[11]


The flavonoids wogonin and baicalein (as well as their glycosides) are commonly seen as the main active ingredients of scutellaria baicalensis, although there are some other unique flavonoids (namely Oroxylin A and K36) that underlie some of the benefits of this plant. Most other bioactives are either in small quantities and not potent enough to be active, or are common structures found in many plants

The main bioactives are highly present in the roots while not in high levels in the aerial parts (stem and leaves).[16][17][11]

Due to having higher concentrations of the unique bioactives, the main part of the plant that is consumed is the root extract


Properties and Preparation

Some plants in traditional chinese medicine are recommended as decoctions (extracts via liquid) involving a brief soaking period followed by boiling or decocting, with the liquid result being drunk as tea.[9] Ideally, for best preparation of scutellaria baicalensis roots (to reach highest levels of flavonoids extracted) it is soaked in 50°C water for 30 minutes in a herb:water ratio of 1:5-10, and optimum pH is slightly acidic (6.67).[9]

The aforementioned optimal conditions have been noted to reduce the glycosides (to 1/70th and 1/13th for baicalin and wogonoside) while increasing levels of the aglycones by 3.5-fold (baicalein) and 3.1-fold (wogonin), due to removing the glucuronide attached to the aglycone.[9]

Proper extractions can increase levels of the aglycones and reduce concentrations of the glycosides, which is due to removal of the glucuronide from the flavonoid





Baicalein itself appears to be well absorbed (Papp of 1.691+/-0.135x10-5cm/s in a Caco-2 model[18]) although it appears to be rapidly glucuronidated and the baicalein glucuronide is sent back into the lumen (to the basal side of the Caco-2 model).[18] Wogonin and Oroxylin A have similarly good absorption initially,[19] and when baicalein is glucuornidation and effluxed it is not reabsorbed.[18]

Efflux of baicalein and other flavonoids (wogonin and oroxylin A) appear to involve MRPs[20] and the inhibitor MK571 (MRP1 inhibitor) is able to block absorption.[19] P-glycoprotein was not involved in the absorption of these flavonoids.[19]

Although the flavonoids (baicalein most researched) appear to be very well researched, they are rapidly metabolized and then effluxed into the intestines and their metabolic products are not reabsorbed

Baicalin appears to involve intestinal microflora for its metabolism into baicalein (via removal of the glucuronide group), as decreasing intestinal microflora alters the kinetics of the flavonoid.[21]

There may be some absorption of the glycoides (baicalin, wogonoside, etc.) in the colon after hydrolysis by intestinal bacteria



Administration of isolated flavonoids at 5mg/kg noted relatively quick absorption and peaks values, with Tmax values being measured at 5.00m (baicalin), 12.0+/-10.4m (wogonin), and 4.33+/-1.15m (oroxylin A) and reaching respectively Cmax values of 1.10+/-0.49µg/mL (baicalin), 0.57+/-0.14µg/mL (wogonin), and 0.24+/-0.08µg/mL (oroxylin A).[22] While oroxylin A had a quick half-life (38.8m), the other two were more delayed (102-155m).[22]

Administration of a mixture of flavonoids sees oroxylin A have an increase in overall AUC by 170% while the AUC values for baicalin and wogonin decrease by 24% and 11.6%.[22] This is thought to be due to the enzymes of metabolism (glucuronidation) competing for substrate and possibly having less affinity for oroxylin A, as there was no apparent inhibition at the level of the transporter.[22]

Although each flavonoid is absorbed on its own, it appears that ingesting multiple flavonoids will reduce the rate of metabolism (possibly via competitive means). Oroxylin A appears to have a greater AUC under these instances, perhaps due to less affinity for the enzymes (which would rather metabolize baicalin and/or wogonin)

Administration of the plant material as a decotion at 8mL/kg (baicalin at 21.1mg/mL, wogonoside at 1.88mg/mL, baicalein at 9.72mg/mL, wogonin at 8.22mg/mL, oroxylin A at 0.62mg/mL and chrysin at 0.23mg/mL) followed a bimodal absorption with a peak after 45 minutes (thought to be due to direct absorption) and then a lesser peak at 8-12 hours (possible related to colonic fermentation).[23] The peaks reached in this study were recorded for baicalein (Cmax of 2228+/-463ng/mL at a Tmax of 0.23+/-0.09h), baicalin (13306+/-2626ng/mL at 0.30+/-0.07h), wogonoside (816.4+/-144.9ng/mL at 0.60+/-0.15h), wogonin (2526+/-378ng/mL at 0.33+/-0.20h), oroxylin A (471.6+/-115.4ng/mL at 0.20+/-0.07h), and chrysin (90.22+/-19.55ng/mL at 0.40+/-0.15h).[23]

Other studies have confirmed somewhat similar peaks in the blood for the main three flavonoids following oral ingestion in rats[24][25] including a standardized extract of PF-2405.[26]

Ingestion of the root of the plant results in increases in serum levels of all measured bioactives, with the peaks for the flavonoids reaching the low micromolar (µM) range



Baicalein does not appear to undergo any hydroxylation of phase I metabolism in liver or intestinal microsomes.[27]

At the same site that baicalin, wogonin, and oroxylin A are initially bound to their glycoside they can also be conjugated by 5'-diphospho-glucuronosyltransferase (UGT) or sulphotransferase (SULT) enzymes in the liver.[27][18] Baicalin is most rapidly conjugated by UGT1A8 and 1A9, although all except 1A3 and 1A7 are active on converting baicalin to baicalin glucuronide.[27]

The flavonoids appears to be readily glucuronidation, which constitutes the major pathway of metabolism

The rate of conjugation appears to be lesser when the three main flavonoids are coingested relative to when they are taken in isolation, which is thought to be due to competition by glucuronidation enzymes.[22] It has been noted elsewhere (baicalin in isolation) that maximal rate of metabolism was at 10µM with higher concentrations having a lower rate, suggesting a saturation point.[27]

As all three main flavonoids are glucuronidated, the rate of glucuronidation any individual flavonoid is lesser when a mixture of all of them are ingested


Neural Kinetics

Baicalin is able to cross the blood brain barrier (injected dose of 24mg/kg) and concentrations detected in cerebrospinal fluid following this dose have reached 344.235+/-71.406μg/L (27% of serum concentration).[28]

Baicalin in the blood can cross the blood brain barrier, although it does not appear to be at the same concentration in the brain and the blood


Enzymatic Interactions

Oroxylin A appears to be able to inhibit the P-glycoprotein (P-gp) transporter in the range of 5-40μM and has shown efficacy at an oral intake of 50mg/kg to rats altering paclitaxel pharmacokinetics.[29]

Oroxylin A, in higher oral doses, appears to be a P-glycoprotein inhibitor

Components of scutellaria baicanelsis are known to interact with adenosine monophosphate kinase (AMPK), a protein involved in energy metabolism and the main target of Berberine and Metformin.[30] AMPK is regulated by both LKB1 (direct phosphorylation and ADP:ATP responsive)[31] and CaMKKβ (intracellular calcium influx and ADP:ATP insensitive)[32] proteins.

Baicalin (the glycoside) has been found to preserve the levels of hepatic AMPK when given intraperitoneally at 80mg/kg, which was credited to abolishing the weight gain on a high-fat diet (the high fat diet was able to reduce AMPK phosphorylation).[33] AMPK has been found to be activated by baicalin in the concentration range of 5-10μM[33] and appears to be due to CaMKKβ rather than LKB1[34] similar to resveratrol,[35] phosphorylation of AMPK has been noted at concentrations as low as 1µM (5µM similar potency) to around 4-fold control levels within an hour.[34]

The activation of AMPK via baicalin does not appear to be associated with ROS production[34] (producing ROS is known to activate AMPK[36][37]) and both wogonin (in vitro)[38] and oral ingestion of scutellaria baicalensis (10-100mg/kg in rats over four weeks)[39] have been noted to increase AMPK phosporylation.

This activation of AMPK has been shown to be responsible for lipid and cholesterol lowering effects of baicalin.[34][33]

Components of scutellaria baicalensis are known to activate AMPK, which may be a link between the lipid lowering and anti-obese actions of this plant




GABAergic neurotransmission

Baicalein appears to be a GABAA receptor agonist, with the glycoside (Baicalin) having no such effect.[40] Its potency is greater than that of chrysin[40] and it has a Ki value of 5.69+/-0.95µM[41] (IC50 of 10.1+/-1.68μM[12]). The glycoside, baicalin, has a weaker Ki value at 77.10+/-4.79µM and IC50 above 100μM.[41] Interestingly, baicalein may only significantly influence GABAA receptors with α2 and α3 subunits[42][43] which can explain anxiolytic properties and the lack of sedative properties.

Wogonin is also a GABAA agonist[44] with a Ki of 2.03+/-0.24µM at the benzodiazepine binding site.[41]

Baicalin is active in inhibiting convulsion at an oral dose of 5mg/kg[40] and wogonin at 5-10mg/kg.[44] Both of which suggest that they are active following oral ingestion.

Baicalein and Wogonin are both potent GABAA agonists, and can activate this receptor. This is thought to mediate some of the depressant and anxiolytic effects of scutellaria baicalensis

5,7,2'-trihydroxy-6,8-dimethoxyflavone (K36) is the most effective GABAA ligand with a Ki of 6.05+/-0.63nM[45] and appears to be a positive allosteric modulator at concentrations of 1nM (EC50 of 24nM), although maximal stimulation of GABAA receptors only reached 54+/-8% of that seen with diazepam (both at 300nM).[45] Elsewhere, K36 has been found to potently outcompete flunitrazepam for binding to the benzodiazepine site with an IC50 of 0.008+/-0.0002μM (8.0+/-0.2nM)[12]

Other flavonoids with affinity for the GABAA receptor include scutellarein which has a Ki for the GABAA receptor of 12.00+/-1.27µM at the benzodiazepine binding site[41] (IC50 of 21.0+/-1.79μM[12])

Beyond the two main flavonoids, K36 appears to be incredibly potent in both enhancing signalling through the benzodiazepine receptor while suppressing maximal signalling

Oroxylin A appears to be a GABAA receptor antagonist (inhibiting the chloride influx[40][46]) at the benzodiazepine binding site and can inhibit binding of flunitrazepam with an IC50 of 1.09+/-0.07µM[47] and elsewhere an IC50 of 0.14+/-0.01µM has been noted;[12] oral ingestion of 3.75-60mg/kg oroxylin A to rats was able to inhibit the effects of diazepam.[47] It has elsewhere blocked the chloride influx induced by muscimol (GABAA agonist)[48][40] and by baicalein.[40]

Oral ingestion of 50mg/kg oroxylin A has shown minor proconvulsive effects in a rat model (typical of GABAA antagonists)[40] and 5mg/kg oroxylin A has shown anti-amnesiac effects attributed to the GABAA receptor antagonism.[46]

Oroxylin A is a relatively effective GABAA antagonist at the benzodiazepine binding site and has been confirmed to be active following oral ingestion, its properties oppose that of baicalein and wogonin


Dopaminergic Neurotransmission

Oroxylin A has shown an ability to block the dopamine transporter (DAT) in a manner similar to methylphenidate, albeit with less potency (similar potency of oroxylin A to atomoxetine).[49] And synthetic derivatives have been made (5,7-Dihydroxy-6-methoxy-4'-phenoxyflavone) with comparable potency than methylphenidate.[50] This is thought to underlie the attention promoting effects observed at 5-10mg/kg oroxylin A (injections) that had a potency similar to 2mg/kg methylphenidate in spontaneous alterations[49] while 1-5mg/kg was slightly less effective at reducing impulsiveness.[49]

Oroxylin A appears to be a dopamine transport inhibitor, similar to methylphenidate (Ritalin) which is thought to underlie the attention-promoting effects


Adrenergic Neurotransmission

Despite inhibiting dopamine uptake, oroxylin A has failed to modify noradrenaline uptake.[49]

No known interactions with adrenergic neurotransmission at this moment in time



Oroxylin A has been noted to increase CREB and BDNF phosphorylation in cognitively injured mice at 5mg/kg oral intake[51] and mice with beta-amyloid induced memory impairments[52] or to 400% of control mice (no cognitive impairment) at 50μM[53] which is due to activating ERK1/2 (an MAPK),[53][53] this is downstream of GABAA antagonism, as it was mimicked by bicuculline, and blocked by inhibiting NMDA receptors.[53][53]

Due to the above mechanisms, oroxylin A has been noted to stimulate neurogenesis in the hippocampus in a dose-dependent manner when administrated for 7-14 days to otherwise normal mice (5-10mg/kg), with 5mg/kg performing equally to 10mg/kg and 14 days not outperforming 7 days.[54]

The inhibition of GABAA receptors seen with oroxylin A seems to indirectly augment NMDA dependent signalling, which then increases the amount of neurogenesis that occurs. This has been confirmed in rodents following oral ingestion of low doses of this molecule

Baicalin can enhance neural stem/progenator cell production and hippocampal dependent neurogenesis in rats following cerebral ischemic injury when injected at 50mg/kg daily for three weeks,[55] which is thought to be related to an upregulation of MASH1 expression at 7.5-30µM.



Heat Shock Protein 70 (HSP70) is an inducible HSP that exert protective effects in neurons[56] with particular efficacy against ischemic damage,[57][58] this neuroprotective property has been noted with baicalin at 200-300mg/kg[59][60][61] and baicalin is known to preserve HSP70 concentrations during ischeia associated with a preservation of ERK phosphorylation (cytoprotective[62][63]) and reducing the phosphorylation of p38 MAPK and JNK (positively mediates cell death[64][63]) resulting in cytoprotective effects.[61]



Microglia are neuronal support cells involved in the immune system that are able to become 'activated' via inflammatory signals[65] and this inflammation is thought to at least contribute towards cognitive decline such as Parkinson's,[66] Alzheimer's,[67] and multiple sclerosis[68] due to the neurotoxicity associated with chronic activation.[69]

Oroxylin A is able to inhibit microglia activation (from LPS) in the concentration range of 10-100µM as assessed by nitric oxide secretion[70][71] is able to prevent STAT1 activation (70-85% inhibition at 50µM) without affecting NF-kB translocation, ultimately resulting in less secretion of inflammatory cytokines.[71] Wogonin is also able to suppress microglia activation, although via suppressing NF-kB at 50µM.[72]

Oroxylin A and wogonin have been implicated in preventing inflammatory responses in brain cells, which are thought to underlie some of the neuroprotective effects

Reductions in microglia activation and the subsequent inflammation have been noted in vivo when rats are fed 100mg/kg of the extract daily during chronic LPS-injections.[73]


Memory and Learning

Scutellaria baicalensis has shown anti-amnesiac and memory promoting properties against ibotenic acid (toxin that mimicks Alzheimer's[74]) at 10-300mg/kg oral intake (30mg/kg being most effective),[75] beta-amyloid proteins,[52] chronic lipopolysaccharide infusion (100mg/kg of the herb daily, 200mg/kg ineffective),[73] gamma irradiation (isolated baicalin),[76] ischemia,[77] and in animal models of aging (35-115mg/kg range).[78][79][80] In regards to reversing age-related amnesia, scutellaria baicalensis (50-200mg/kg) is slightly more potent than the comparator of 200mg/kg piracetam over 47 days.[80]

Scutellaria baicalensis appears to have anti-amnesiac properties that are quite general

One study assessing the anti-amnesiac properties of Oroxylin A against scopolamine conducted a test in otherwise normal young mice, and while 2.5-20mg/kg trended to improve cognition (passive avoidance) only 5-10mg/kg reached statistical significance.[46]

Some evidence to support the usage of Oroxylin A in improving cognition in otherwise healthy and young rodents, suggesting nootropic effects



20mg/kg of baicalin to rats (prodrug for baicalein, a GABAA agonist) has failed to significantly affect locomotor activity[40] and 10mg/kg wogonin also appears to be ineffective.[44] Even the potent GABAA modulator K36 at 1-8mg/kg (injections) has failed to alter locomotion despite conferring anxiolytic properties.[45]

Intracerebral injections of baicalein have shown sedative properties in augmenting sleep time (108-120% of control), while benzodiazepine antagonists failed to abolish the effects in one study[81] yet were successful in preventing the increase in sleep time in the other study.[82] Both slow-wave sleep and REM sleep appear to be increased with baicalin administration prior to dark phase sleep (nighttime sleeping).[82]

Sleep induced in light phases (equivalent of daytime) seems to actually be hindered by baicalin, thought to be from interfering with an IL-1β induced slow wave sleep enhancement.[82]



Baicalein has shown anxiolytic properties in a rat conflict test due to binding to the benzodiazepine binding site of the GABAA receptor[83]

GABAA receptors with α2 and α3 subunits are implicated (as they are the target of baicalein[42][43]).



In spontaneously hypertensive rats (also a model for attention deficits thought to be related to altered dopamine transportation[84]) oroxylin A appears to improve attention[48][49] thought to be related to its ability to block the dopamine transporter.[49]

Oroxylin A may have attention-promoting properties due to its inhibition of the dopamine transporter, a mechanism similar to methylphenidate (ritalin)


Cardiovascular Health



Baicalin has been shown to stimulate nitric oxide production in isolated HUVECs (endothelial cells) via activating eNOS in the range of 50-200nM with 50nM outperforming 10nM bradykinin (comparator).[1] Baicalein, wogonin, and wogonoside appear to be inactive on eNOS in the 10-200nM range,[1] suggesting that the glucuronide group of baicalin is required.

This may be biologically relevant as some evidence suggest a hypothermic effect due to cutaneous vasodilatation in a dose-dependent manner.[85]

Baicalin (the glycoside, aglycone is inactive) appears to be a potent eNOS inducer and potentially can increase nitric oxide. This may be relevant after oral ingestion due to the low concentration required


Triglycerides and Cholesterol

Components of scutellaria baicalensis have demonstrated lipid and cholesterol lowering effects secondary to AMPK activation in vitro.[34][33]

May have lipid lowering properties in animals due to activation of AMPK, a known lipid lowering mechanism of action


Interactions with Glucose Metabolism



Due to the ability of both Wogonin[38] and Baicalin[33] (as well as the whole plant extract[39]) to activate AMPK, scutellaria baicalensis has some evidence investigating its interactions with glucose metabolism. This is since AMPK activation is inhernetly hypoglycemic[30] and the molecular target of many anti-diabetic compounds (Metformin and Berberine in particular).

Scutellaria baicalensis may have anti-diabetic properties due to its ability to activate AMPK


Blood Glucose

In studies of diabetic mice, 10-100mg/kg of the plant extract (11.02% baicalin, 1.40% baicalein, and 0.39% wogonin) has been found to dose-dependently reduce circulating insulin concentrations over four weeks[39] which has been replicated with 400mg/kg of the plant over the same timeframe with a potency nonsignificantly greater than 500mg/kg metformin.[86]

50mg/kg of scutellaria baicalensis (20.46% baicalin, 0.93% baicalein, and 0.33% wogonin) or 5mg/kg of isolated baicalin have elsewhere failed to reduce blood glucose in diabetic rats[87] although 400mg/kg appears to be as effective as the reference drug (500mg/kg metformin).[86]

This plant may reduce blood glucose, although it appears to require a few weeks to be effective. It seems to be more effective in reducing insulin than in reducing glucose


Obesity and Fat Mass



PPARα is a target that regulates fatty acid synthesis and oxidation[88] and are thought to be a druggable target to treat obesity,[89] the activation of PPARα is known to be beneficial for obesity as it increases fatty acid oxidation while suppressing synthesis.[90]

Scutellarin is able to suppress adipocyte differentiation at 100μM (but not 50μM) associated with downregulation of adipogenic transcription factors (PPARγ and C/EBPα, no influence on C/EBPβ) and upregulation of PPARα and no influence on PPARδ.[91] Scutellarin was found to bind to PPARα, although its affinity was not determined.[91] Wogonin has been found to also activate PPARα as well as AMPK.[38]

It is possible that flavonoids in scutellaria baicalensis can activate a protein called PPARα and thus cause fat burning, but this is currently not well investgiated following oral ingestion (and occurs at fairly high concentrations)



Intraperitoneal injections of 80mg/kg baicalein daily for 16 weeks was able to inhibit the fat gain caused by a high-fat diet in rats, which is thought to be secondary to AMPK activation in the liver.[33] In diabetic mice (db/db) given 10mg/kg or 100mg/kg of scutellaria baicalensis (11.02% baicalin) extract daily for four weeks, supplementation was able to dose-dependently reduce the observed weight gain,[39] again thought to be due to AMPK activation.

Minimal evidence, but either isolated flavonoids or the root extract itself can reduce weight gain which is thought to be secondary to AMPK activation. No studies have yet assessed fat loss per se


Inflammation and Immunology



PHA-activated PBMCs are significantly suppressed to near undetectable levels (1.9% of control) with 50-200µg/mL of the ethanolic extract.[7]



Scutellaria baicalensis shows moderate anti-inflammatory effects on LPS-induced macrophage activation, with the ethanolic root extract (8.53% baicalin) reducing nitric oxide production to 8.85% of control at 800µg/mL and 54.6% at 200µg/mL (outperformed only by Schizonepeta tenuifolia).[7] The water extract had minimal inhibition[7] and has elsewhere shown a potency (50-400µg/mL) comparable to 25µM gallic acid.[2]

Isolated compounds from this plant have inhibited LPS-induced macrophage activation, including baicalein (66.4+/-1µM), wogonin (45.3+/-0.2µM), and oroxylin A (58.2+/-0.6µM)[3] with the latter also effective in other tissues via inhibition of NF-kB[92][93] to near control levels in the range of 5-20µg/mL oroxylin A.[94]

When looking at the mechanisms it appears that baicalein activates the estrogen receptor on macrophages[95] similar to oroxylin A (in the range of 10nM to 10µM).[96] When the estrogen receptor is activated on macrophages it causes antiinflammatory effects via suppressing NF-kB activation[97] and the effects of both baicalein and oroxylin A are blocked when estrogen signalling is blocked.[95][96]

Baicalein and Oroxylin A are both antiinflammatory agents on macrophages, and this appears to be secondary to them acting on the estrogen receptors and causing suppression of NF-kB activation


Viral and Bacterial Interaction

Baicalin is known to inhibit HIV replication[98] with a potency in the range of 43.27-47.34μM[99] and is more potent when bound to zinc (29.08-31.17μM).[99]

Anti-bacterial effects from baicalin have been noted against Staphylococcus aureus induced pneumonia where the bacteria secreted α-Hemolysin (a polypeptide that aids in infection[100][101]) is interfered with in vitro (IC50 of 6.63μg/mL) and following injections of 25-100mg/kg baicalin alongside the bacteria in mice.[102] It appears that baicalin can directly bind to α-Hemolysin in the latter's binding cavity which interfers with its ability to bind to cells, and may extend to wogonin (IC50 of 10.27μg/mL) but not scutellarin.[102]



An ethanolic extract of scutellaria baicalensis (5.7% baicalin) given to rats 48 hours prior to an allergic challenge (compound 48/80) at 280mg/kg bodyweight was able to exert a mild antiallergic action relative to control (about 6.6%)[103] despite stronger actions in vitro where 1-100μg/mL caused a near halving of histamine release with most potency at 10μg/mL.[103]

There appears to be a possible suppressive effect on histamine release with scutellaria baicalensis, although the current oral evidence in rats did not suggest a large degree of efficacy



An injection of 20mg/kg isolated wogonin appears to be more effective at reducing carrageenaan-induced paw edema (82.9%) than ibuprofen.[3]


Nutrient-Nutrient Interactions



Scutellaria baicalensis (400mg/kg of 29.6% baicalin) in combination with the anti-diabetic drug Metformin (500mg/kg) in diabetic rats noted that all three groups (either drug in isolation plus the combination) were equally effective in reducing blood glucose and triglycerides over four weeks although they appeared to be additive in increasing pancreatic insulin concentrations and antioxidant status.[86]

Although there is no evidence that Scutellaria baicalensis enhances the anti-diabetic effects of Metformin, it appears to aid with antioxidant status of diabetic rats and thus may be complementary


Interactions with Organ Systems


Male Sex Organs

An ethanolic extract of Scutellaria baicalensis is able to induce relaxation in the corpus cavernosum in a concentration dependent manner reaching 89.85+/-9.97% relaxation at 300µg/mL.[15] This is inhibited by nitric oxide and cGMP inhibitors, and is involved with potassium channels (regulator of blood flow in this tissue[104] as channel openers cause relaxation[105]) but independent of muscarininc and adrenergic receptors.[15]

1.^Chen Z, Nihei K, Tanaka H, Uda Y, Kabuyama YIdentification of a nitric oxide generation-stimulative principle in Scutellariae radixBiosci Biotechnol Biochem.(2013)
2.^Yoon SB, Lee YJ, Park SK, Kim HC, Bae H, Kim HM, Ko SG, Choi HY, Oh MS, Park WAnti-inflammatory effects of Scutellaria baicalensis water extract on LPS-activated RAW 264.7 macrophagesJ Ethnopharmacol.(2009 Sep 7)
4.^Ho FM, Liao YH, Yang AJ, Lee Chao PD, Hou YC, Huang CT, Lin SR, Lee KR, Huang KC, Lin WWAnti-atherosclerotic action of Ger-Gen-Chyn-Lian-Tang and AMPK-dependent lipid lowering effect in hepatocytesJ Ethnopharmacol.(2012 Jun 26)
5.^Lee JJ, Kim T, Cho WK, Ma JYAntithrombotic and antiplatelet activities of Soshiho-tang extractBMC Complement Altern Med.(2013 Jun 18)
7.^Yue GG, Chan BC, Kwok HF, To MH, Hon KL, Fung KP, Lau CB, Leung PCScreening for anti-inflammatory and bronchorelaxant activities of 12 commonly used Chinese herbal medicinesPhytother Res.(2012 Jun)
8.^Huang WH, Chien PY, Yang CH, Lee ARNovel synthesis of flavonoids of Scutellaria baicalensis GeorgiChem Pharm Bull (Tokyo).(2003 Mar)
9.^Yu C, Qu F, Mao Y, Li D, Zhen Z, Nass R, Calway T, Wang Y, Yuan CS, Wang CZDifferent extraction pretreatments significantly change the flavonoid contents of Scutellaria baicalensisPharm Biol.(2013 Jun 5)
11.^Liu G, Rajesh N, Wang X, Zhang M, Wu Q, Li S, Chen B, Yao SIdentification of flavonoids in the stems and leaves of Scutellaria baicalensis GeorgiJ Chromatogr B Analyt Technol Biomed Life Sci.(2011 Apr 15)
14.^Kimura Y, Okuda H, Tani T, Arichi SStudies on Scutellariae radix. VI. Effects of flavanone compounds on lipid peroxidation in rat liverChem Pharm Bull (Tokyo).(1982 May)
15.^Li X, Oh HC, Son SB, Lee YJ, Kang DG, Lee HSEffect of an Ethanol Extract of Scutellaria baicalensis on Relaxation in Corpus Cavernosum Smooth MuscleEvid Based Complement Alternat Med.(2012)
20.^Zhang L, Lin G, Kovács B, Jani M, Krajcsi P, Zuo ZMechanistic study on the intestinal absorption and disposition of baicaleinEur J Pharm Sci.(2007 Jul)
21.^Kang MJ, Ko GS, Oh DG, Kim JS, Noh K, Kang W, Yoon WK, Kim HC, Jeong HG, Jeong TCRole of metabolism by intestinal microbiota in pharmacokinetics of oral baicalinArch Pharm Res.(2013 Jun 18)
22.^Li CR, Zhang L, Wo SK, Zhou LM, Lin G, Zuo ZPharmacokinetic interactions among major bioactive components in Radix Scutellariae via metabolic competitionBiopharm Drug Dispos.(2012 Dec)
24.^Kim YH, Jeong DW, Paek IB, Ji HY, Kim YC, Sohn DH, Lee HSLiquid chromatography with tandem mass spectrometry for the simultaneous determination of baicalein, baicalin, oroxylin A and wogonin in rat plasmaJ Chromatogr B Analyt Technol Biomed Life Sci.(2006 Dec 5)
30.^Hardie DG, Ross FA, Hawley SAAMPK: a nutrient and energy sensor that maintains energy homeostasisNat Rev Mol Cell Biol.(2012 Mar 22)
31.^Woods A, Johnstone SR, Dickerson K, Leiper FC, Fryer LG, Neumann D, Schlattner U, Wallimann T, Carlson M, Carling DLKB1 is the upstream kinase in the AMP-activated protein kinase cascadeCurr Biol.(2003 Nov 11)
32.^Hurley RL, Anderson KA, Franzone JM, Kemp BE, Means AR, Witters LAThe Ca2+/calmodulin-dependent protein kinase kinases are AMP-activated protein kinase kinasesJ Biol Chem.(2005 Aug 12)
33.^Guo HX, Liu DH, Ma Y, Liu JF, Wang Y, Du ZY, Wang X, Shen JK, Peng HLLong-term baicalin administration ameliorates metabolic disorders and hepatic steatosis in rats given a high-fat dietActa Pharmacol Sin.(2009 Nov)
34.^Ma Y, Yang F, Wang Y, Du Z, Liu D, Guo H, Shen J, Peng HCaMKKβ is involved in AMP-activated protein kinase activation by baicalin in LKB1 deficient cell linesPLoS One.(2012)
35.^Park SJ, Ahmad F, Philp A, Baar K, Williams T, Luo H, Ke H, Rehmann H, Taussig R, Brown AL, Kim MK, Beaven MA, Burgin AB, Manganiello V, Chung JHResveratrol ameliorates aging-related metabolic phenotypes by inhibiting cAMP phosphodiesterasesCell.(2012 Feb 3)
36.^Toyoda T, Hayashi T, Miyamoto L, Yonemitsu S, Nakano M, Tanaka S, Ebihara K, Masuzaki H, Hosoda K, Inoue G, Otaka A, Sato K, Fushiki T, Nakao KPossible involvement of the alpha1 isoform of 5'AMP-activated protein kinase in oxidative stress-stimulated glucose transport in skeletal muscleAm J Physiol Endocrinol Metab.(2004 Jul)
37.^Mungai PT, Waypa GB, Jairaman A, Prakriya M, Dokic D, Ball MK, Schumacker PTHypoxia triggers AMPK activation through reactive oxygen species-mediated activation of calcium release-activated calcium channelsMol Cell Biol.(2011 Sep)
38.^Bak EJ, Kim J, Choi YH, Kim JH, Lee DE, Woo GH, Cha JH, Yoo YJWogonin ameliorates hyperglycemia and dyslipidemia via PPARα activation in db/db miceClin Nutr.(2013 Mar 26)
39.^Song KH, Lee SH, Kim BY, Park AY, Kim JYExtracts of Scutellaria baicalensis reduced body weight and blood triglyceride in db/db MicePhytother Res.(2013 Feb)
40.^Yoon SY, dela Peña IC, Shin CY, Son KH, Lee YS, Ryu JH, Cheong JH, Ko KHConvulsion-related activities of Scutellaria flavones are related to the 5,7-dihydroxyl structuresEur J Pharmacol.(2011 Jun 1)
42.^Xu Z, Wang F, Tsang SY, Ho KH, Zheng H, Yuen CT, Chow CY, Xue HAnxiolytic-Like Effect of baicalin and its additivity with other anxiolyticsPlanta Med.(2006 Feb)
43.^Wang F, Xu Z, Ren L, Tsang SY, Xue HGABA A receptor subtype selectivity underlying selective anxiolytic effect of baicalinNeuropharmacology.(2008 Dec)
44.^Park HG, Yoon SY, Choi JY, Lee GS, Choi JH, Shin CY, Son KH, Lee YS, Kim WK, Ryu JH, Ko KH, Cheong JHAnticonvulsant effect of wogonin isolated from Scutellaria baicalensisEur J Pharmacol.(2007 Nov 28)
45.^Huen MS, Hui KM, Leung JW, Sigel E, Baur R, Wong JT, Xue HNaturally occurring 2'-hydroxyl-substituted flavonoids as high-affinity benzodiazepine site ligandsBiochem Pharmacol.(2003 Dec 15)
46.^Kim DH, Jeon SJ, Son KH, Jung JW, Lee S, Yoon BH, Lee JJ, Cho YW, Cheong JH, Ko KH, Ryu JHThe ameliorating effect of oroxylin A on scopolamine-induced memory impairment in miceNeurobiol Learn Mem.(2007 May)
49.^Yoon SY, dela Peña I, Kim SM, Woo TS, Shin CY, Son KH, Park H, Lee YS, Ryu JH, Jin M, Kim KM, Cheong JHOroxylin A improves attention deficit hyperactivity disorder-like behaviors in the spontaneously hypertensive rat and inhibits reuptake of dopamine in vitroArch Pharm Res.(2013 Jan)
50.^Dela Peña IC, Young Yoon S, Kim Y, Park H, Man Kim K, Hoon Ryu J, Young Shin C, Hoon Cheong J5,7-Dihydroxy-6-methoxy-4'-phenoxyflavone, a derivative of oroxylin A improves attention-deficit/hyperactivity disorder (ADHD)-like behaviors in spontaneously hypertensive ratsEur J Pharmacol.(2013 May 23)
51.^Kim DH, Jeon SJ, Son KH, Jung JW, Lee S, Yoon BH, Choi JW, Cheong JH, Ko KH, Ryu JHEffect of the flavonoid, oroxylin A, on transient cerebral hypoperfusion-induced memory impairment in micePharmacol Biochem Behav.(2006 Nov)
52.^Kim DH, Kim S, Jeon SJ, Son KH, Lee S, Yoon BH, Cheong JH, Ko KH, Ryu JHThe effects of acute and repeated oroxylin A treatments on Abeta(25-35)-induced memory impairment in miceNeuropharmacology.(2008 Oct)
53.^Jeon SJ, Rhee SY, Seo JE, Bak HR, Lee SH, Ryu JH, Cheong JH, Shin CY, Kim GH, Lee YS, Ko KHOroxylin A increases BDNF production by activation of MAPK-CREB pathway in rat primary cortical neuronal cultureNeurosci Res.(2011 Mar)
54.^Lee S, Kim DH, Lee DH, Jeon SJ, Lee CH, Son KH, Jung JW, Shin CY, Ryu JHOroxylin A, a flavonoid, stimulates adult neurogenesis in the hippocampal dentate gyrus region of miceNeurochem Res.(2010 Nov)
55.^Zhuang PW, Cui GZ, Zhang YJ, Zhang MX, Guo H, Zhang JB, Lu ZQ, Isaiah AO, Lin YXBaicalin regulates neuronal fate decision in neural stem/progenitor cells and stimulates hippocampal neurogenesis in adult ratsCNS Neurosci Ther.(2013 Mar)
56.^Giffard RG, Yenari MAMany mechanisms for hsp70 protection from cerebral ischemiaJ Neurosurg Anesthesiol.(2004 Jan)
57.^Rajdev S, Hara K, Kokubo Y, Mestril R, Dillmann W, Weinstein PR, Sharp FRMice overexpressing rat heat shock protein 70 are protected against cerebral infarctionAnn Neurol.(2000 Jun)
58.^Tsuchiya D, Hong S, Matsumori Y, Kayama T, Swanson RA, Dillman WH, Liu J, Panter SS, Weinstein PROverexpression of rat heat shock protein 70 reduces neuronal injury after transient focal ischemia, transient global ischemia, or kainic acid-induced seizuresNeurosurgery.(2003 Nov)
59.^Zhang ZJ, Li P, Wang Z, Li PT, Zhang WS, Sun ZH, Zhang XJ, Wang YYA comparative study on the individual and combined effects of baicalin and jasminoidin on focal cerebral ischemia-reperfusion injuryBrain Res.(2006 Dec 6)
60.^Zhang ZJ, Wang Z, Zhang XY, Ying K, Liu JX, Wang YYGene expression profile induced by oral administration of baicalin and gardenin after focal brain ischemia in ratsActa Pharmacol Sin.(2005 Mar)
63.^Xia Z, Dickens M, Raingeaud J, Davis RJ, Greenberg MEOpposing effects of ERK and JNK-p38 MAP kinases on apoptosisScience.(1995 Nov 24)
64.^Oppenheim RWCell death during development of the nervous systemAnnu Rev Neurosci.(1991)
65.^Glass CK, Saijo K, Winner B, Marchetto MC, Gage FHMechanisms underlying inflammation in neurodegenerationCell.(2010 Mar 19)
68.^Takeuchi H, Wang J, Kawanokuchi J, Mitsuma N, Mizuno T, Suzumura AInterferon-gamma induces microglial-activation-induced cell death: a hypothetical mechanism of relapse and remission in multiple sclerosisNeurobiol Dis.(2006 Apr)
69.^Block ML, Zecca L, Hong JSMicroglia-mediated neurotoxicity: uncovering the molecular mechanismsNat Rev Neurosci.(2007 Jan)
70.^Pham TA, Che H, Phan PT, Lee JW, Kim SS, Park HOroxylin A analogs exhibited strong inhibitory activities against iNOS-mediated nitric oxide (NO) productionBioorg Med Chem Lett.(2012 Apr 1)
72.^Lee H, Kim YO, Kim H, Kim SY, Noh HS, Kang SS, Cho GJ, Choi WS, Suk KFlavonoid wogonin from medicinal herb is neuroprotective by inhibiting inflammatory activation of microgliaFASEB J.(2003 Oct)
75.^Heo H, Shin Y, Cho W, Choi Y, Kim H, Kwon YKMemory improvement in ibotenic acid induced model rats by extracts of Scutellaria baicalensisJ Ethnopharmacol.(2009 Feb 25)
79.^Jeong K, Shin YC, Park S, Park JS, Kim N, Um JY, Go H, Sun S, Lee S, Park W, Choi Y, Song Y, Kim G, Jeon C, Park J, Lee K, Bang O, Ko SGEthanol extract of Scutellaria baicalensis Georgi prevents oxidative damage and neuroinflammation and memorial impairments in artificial senescense miceJ Biomed Sci.(2011 Feb 8)
82.^Chang HH, Yi PL, Cheng CH, Lu CY, Hsiao YT, Tsai YF, Li CL, Chang FCBiphasic effects of baicalin, an active constituent of Scutellaria baicalensis Georgi, in the spontaneous sleep-wake regulationJ Ethnopharmacol.(2011 May 17)
83.^Liao JF, Hung WY, Chen CFAnxiolytic-like effects of baicalein and baicalin in the Vogel conflict test in miceEur J Pharmacol.(2003 Mar 19)
89.^Evans RM, Barish GD, Wang YXPPARs and the complex journey to obesityNat Med.(2004 Apr)
92.^Tseng TL, Chen MF, Tsai MJ, Hsu YH, Chen CP, Lee TJOroxylin-A rescues LPS-induced acute lung injury via regulation of NF-κB signaling pathway in rodentsPLoS One.(2012)
93.^Yao J, Hu R, Sun J, Lin B, Zhao L, Sha Y, Zhu B, You QD, Yan T, Guo QLOroxylin A prevents inflammation-related tumor through down-regulation of inflammatory gene expression by inhibiting NF-κB signalingMol Carcinog.(2012 Sep 4)
95.^Fan GW, Zhang Y, Jiang X, Zhu Y, Wang B, Su L, Cao W, Zhang H, Gao XAnti-inflammatory Activity of Baicalein in LPS-Stimulated RAW264.7 Macrophages via Estrogen Receptor and NF-κB-Dependent PathwaysInflammation.(2013 Jul 28)
96.^Wang H, Guo Y, Zhao X, Li H, Fan G, Mao H, Miao L, Gao XAn estrogen receptor dependent mechanism of oroxylin a in the repression of inflammatory responsePLoS One.(2013 Jul 29)
97.^Cutolo M, Sulli A, Seriolo B, Accardo S, Masi ATEstrogens, the immune response and autoimmunityClin Exp Rheumatol.(1995 Mar-Apr)
98.^Li BQ, Fu T, Yan YD, Baylor NW, Ruscetti FW, Kung HFInhibition of HIV infection by baicalin--a flavonoid compound purified from Chinese herbal medicineCell Mol Biol Res.(1993)
99.^Wang Q, Wang YT, Pu SP, Zheng YTZinc coupling potentiates anti-HIV-1 activity of baicalinBiochem Biophys Res Commun.(2004 Nov 12)
102.^Qiu J, Niu X, Dong J, Wang D, Wang J, Li H, Luo M, Li S, Feng H, Deng XBaicalin protects mice from Staphylococcus aureus pneumonia via inhibition of the cytolytic activity of α-hemolysinJ Infect Dis.(2012 Jul 15)
103.^Jung HS, Kim MH, Gwak NG, Im YS, Lee KY, Sohn Y, Choi H, Yang WMAntiallergic effects of Scutellaria baicalensis on inflammation in vivo and in vitroJ Ethnopharmacol.(2012 May 7)
104.^Christ GJ, Spray DC, Brink PRCharacterization of K currents in cultured human corporal smooth muscle cellsJ Androl.(1993 Sep-Oct)