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Objective: To investigate the effect of wogonin (WOG) on hypoxia/reoxygenation (H/R)-induced cardiomyocyte apoptosis by regulating adenosine monophosphate-activated protein kinase (AMPK)/NOD-like receptor protein 3 (NLRP3) signaling pathway. Methods: H9C2 cells were divided into Control group (normal culture), H/R group (H/R induction), L (low dose)-WOG group, M (medium dose)-WOG group, H (high dose)-WOG group (40, 80, 120 µmol/L WOG were added on the basis of H/R induction), WOG+Compound C group (10 µmol/L AMPK inhibitor Compound C was added on the basis of H-WOG group). The effect of WOG on the proliferation of H9C2 cells was detected by methyl thiazolyl tetrazolium (MTT) assay and 5-ethynyl-2'-deoxyuridine (EdU) staining. The effect of WOG on apoptosis of H9C2 cells was detected by flow cytometry. The levels of serum oxidative stress indexes [malondialdehyde (MDA), reactive oxygen species (ROS), superoxide dismutase (SOD)] and inflammatory factors [interleukin (IL)-1B, IL-18] in H9C2 cells were detected by enzyme-linked immunosorbent assay (ELISA). The expression of AMPK, NLRP3, B cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) in H9C2 cells was detected by Western blot (WB). Results: The optical density (OD), EdU positive cell rate, SOD, AMPK and Bcl-2 of H9C2 cells in H/R group were lower than those in Control group, and the apoptosis rate, IL-1B, IL-18, ROS, MDA, NLRP3 and Bax were higher than those in Control group (P<0.05). Compared with H/R group, OD490, EdU positive cell rate, SOD, AMPK and Bcl-2 expression in L-WOG group, M-WOG group and H-WOG group increased, while apoptosis rate, IL-1B, IL-18, ROS, MDA, NLRP3 and Bax decreased (P<0.05). The OD, EdU positive cell rate, SOD, AMPK and Bcl-2 in WOG+Compound C group were lower than those in H-WOG group, and the apoptosis rate, IL-1B, IL-18, ROS, MDA, NLRP3 and Bax expression were higher than those in H-WOG group (P<0.05). Conclusion: WOG can inhibit H/R-induced cardiomyocyte apoptosis, which may be relate to the AMPK/NLRP3 signaling pathway. [ABSTRACT FROM AUTHOR]

Background Hepatocellular carcinoma (HCC) is the leading cause of cancer-related deaths. The current prevention and treatment situation remains critical. It is of scientific significance to explore new therapeutic agents for HCC. Objective To analyze the mechanism of wogonin on HCC by network pharmacology and to verify it in vitro. Methods The drug targets of wogonin were searched in TCMSP database, and the disease targets of HCC were collected from TTD, GenCard, OMIM, DisGent databases. The collected drug targets and disease targets were intersected as potential targets for drug intervention in diseases. R software was used for enrichment analysis of intersection targets, STRING database and Cytoscape software were used to construct protein interaction network and screen core targets. The core targets were further analyzed in GIEPA database. Finally, the preliminary analysis results were verified by in vitro experiments, including cell activity determination using CCK-8 kit, cell proliferation determination using plate clone formation experiment, cell migration determination using scoring test, protein expression level determination using Western-blotting (WB) assay. Results The AMDE characteristics of wogonin were found to be in accordance with the rules for small molecule drug formation and the toxicity analysis showed no toxicity. A total of 135 wogonin targets and 8 238 HCC targets were collected, and 113 targets were intersected. Through the analysis of the core genes of TOP10 screened by the constructed protein interaction network, it was found that the mRNA levels of CDK1 and SRC in liver cancer tissues were higher than those in normal liver tissues (P

BACKGROUND: Rheumatoid arthritis is an inflammatory disease. Many studies have shown that wogonin has a good anti-inflammatory effect on rheumatoid arthritis, but its exact efficacy and specific mechanism of action remain to be clarified. OBJECTIVE: To investigate the mechanism of wogonin ameliorating joint inflammation by regulating endoplasmic reticulum stress pathway in rats with collagen- induced arthritis. METHODS: (1) At the animal level: Female Wistar rats were divided into healthy control group, arthritis model group and wogonin treatment group. Rat models of arthritis in the latter two groups were established by subcutaneous injection of bovine type II collagen and adjuvant. In the wogonin group, wogonin was given by gavage for 28 consecutive days after modeling. During this period, the rats in each group were weighed, and arthritis score and ankle swelling were measured every 7 days. After the experiment, the pathological changes of the joint were observed, the mRNA and protein levels of endoplasmic reticulum stress pathway GRP78 and CHOP were detected by qRT-PCR, western blot, and immunohistochemistry. (2) At the cellular level, cell counting kit-8 was used to detect the cytotoxic effect of wogonin on fibroblast-like synoviocytes from rats with collagen-induced arthritis. The fibroblast-like synoviocytes induced by thapsigargin were treated with different concentrations of wogonin. The levels of interleukin-1β and tumor necrosis factor-α in the cell supernatant were detected by ELISA, and the intracellular reactive oxygen species in each group were determined by DCFH-DA probe method. The mRNA and protein levels of GRP78, IRE1α, XBP1s and CHOP were detected by qRT-PCR and western blot, respectively. RESULTS AND CONCLUSION: Compared with the healthy control group, arthritis index score and ankle swelling degree in the arthritis model group were increased (P < 0.01), synovial hyperplasia, inflammatory cell infiltration, cartilage destruction and bone erosion were observed in pathological sections, and the mRNA and protein expressions of GRP78 and CHOP in the ankle were significantly increased (P < 0.01), which were mainly located in synovial tissue and articular surface. Compared with the arthritis model group, the arthritis index score and ankle swelling degree in the wogonin treatment group were decreased (P < 0.05), synovial hyperplasia and the number of inflammatory cells were decreased, cartilage destruction and bone erosion were alleviated, the mRNA and protein expression levels of GRP78 and CHOP in the ankle were decreased (P < 0.05), particularly in synovial tissue and on the articular surface. There was no significant difference in body mass among the three groups (P > 0.05). In the cell experiment, 200 μmol/L wogonin significantly reduced the survival rate of fibroblast-like synoviocytes (P < 0.01). Compared with the blank control group, the levels of interleukin-1β, tumor necrosis factor-α, content of reactive oxygen species, and mRNA and protein expression of GRP78, IRE1α, XBP1s, and CHOP in the thapsigargin group were significantly increased (P < 0.05); compared with the thapsigargin group, 50 and 100 μmol/L wogonin significantly reduced the levels of interleukin-1β and tumor necrosis factor-α in the cell supernatant (P < 0.05, P < 0.01), and 100 μmol/L wogonin significantly reduced the content of reactive oxygen species (P < 0.01) and down-regulated the mRNA and protein expression levels of GRP78, IRE1α, XBP1s and CHOP (all P < 0.05). These results suggest that wogonin can effectively alleviate joint inflammatory responses in rats with collagen-induced arthritis, and the endoplasmic reticulum stress pathway may be the key target of its intervention. [ABSTRACT FROM AUTHOR]

AIM: To investigate the mechanism by which wogonin (WOG) induces ferroptosis in collagen-induced arthritis rat fibroblast-like synoviocytes (rat CIA-FLS cells) through the nuclear factor E2-related factor 2 (NRF2)/heme oxygenase-1 (HO-1) signaling pathway. METHODS: Rat CIA-FLS cells were divided into: control group, low, medium, and high dose of (25, 50 and 100 μmol/L) WOG group, ferroptosis inhibitor (LIP-1) group, LIP-1 + high dose WOG group, HO-1 agonist cobalt protoporphyrin (COPP) group, and COPP + high dose WOG group. CCK-8 assay was used for cell viability. Crystal violet staining was used for for cell morphology. The levels of oxidative stress markers glutathione (GSH), malondialdehyde (MDA), and superoxide dismutase (SOD) were measured. DCFH-DA fluorescent probe was used to detect the intracellular reactive oxygen species (ROS) content as well as Western blot to detect the protein expression levels of Kelch-like ECH-associated protein 1 (KEAP-1), NRF2 and HO-1. RESULTS: Compared with the normal control group, administration of WOG treatment resulted in a significant decrease in CIA-FLS cell viability (P< 0. 01, a significant increase in the level of oxidative stress (P<0. 01), a significant increase in the content of ROS (P< 0. 01), a significant decrease in the level of expression of NRF2 and HO-1 proteins (P<0. 01), and a significant increase in the level of KEAP-1 (P<0. 01) in the rat. Compared with the WOG group, the LIP-1-treated group showed a significant increase in cell viability (P<0. 01, a significant decrease in the level of oxidative stress (P<0. 01), and a significant decrease in the content of ROS (P<0. 01). Compared with the WOG group, the addition of COPP resulted in a significant increase in the protein expression levels of NRF2 and HO-1 (P<0. 01) and a significant decrease in KEAP-1 levels (P< 0.01). CONCLUSION: WOG can induce ferroptosis in rat CIA-FLS cells by promoting oxidative stress through the NRF2/HO-1 signaling pathway. [ABSTRACT FROM AUTHOR]

Objective To investigate the impacts of wogonin (WG) on Th17/Treg cell balance in autoimmune hepatitis (AIH) rats. Methods A total of 10 rats were randomly selected as the control group. The remaining rats were injected with concanavalin A (ConA, 12.5 mg/kg) solution via tail vein to construct AIH model rat, which were randomly divided into AIH group, L-WG group (10 mg/kg), M-WG group (20 mg/kg), H-WG group (30 mg/kg), H-WG+VPA group (30 mg/kg WG+300 mg/kg Notch signal pathway activator VPA), 10 rats in each group and administered once a day for 10 days. Serum inflammatory factors and liver function indexes were detected by ELISA; HE staining was used to observe the pathological morphology of liver tissue; the level of spleen Th17/Treg cells was detected by flow cytometry; Western blot was used to detect the expression of spleen retinoid acid related orphan receptor γ t (RORγt), fork head box protein P3 (Foxp3) and liver Notch signal pathway proteins. Results The liver tissue structure of control group was normal and the staining was clear; In AIH group, the cells of liver tissue showed edema, the increase of cell volume led to the compression and narrowing of liver sinuses, and a large number of inflammatory cell infiltration and a small amount of necrosis occurred. The contents of alanine aminotransferase (ALT), aspartate aminotransferase (AST), interleukin (IL)-17 and IL-23, level of Th17 cells, Th17/Treg, the expression of RORγt, Notch, hes family bHLH transcription factor 1 gene (HES1) and hes related family bHLH transcription factor with YRPW motif 1 (HEY1) protein in AIH group were greatly higher than those in control group (P＜0.05), the contents of IL-10 and TNF-β, level of Treg cells, and level of Foxp3 protein were greatly lower(P＜0.05); Compared with AIH group, the liver injury in L-WG group, M-WG group and H-WG group was improved, the contents of ALT, AST, IL-17 and IL-23, level of Th17 cells, Th17/Treg, the expression of RORγt, Notch, HES1 and HEY1 protein were greatly lower (P＜0.05), the contents of IL-10 and TNF-β, level of Treg cells, and level of Foxp3 protein were greatly higher (P＜0.05); VPA reversed the improvement effect of H-WG on AIH rats. Conclusions WG could promote Th17/Treg cell balance in AIH rats by down-regulating Notch signal pathway.

Objective To investigate the impacts of wogonin (WG) on Th17/Treg cell balance in autoimmune hepatitis (AIH) rats. Methods A total of 10 rats were randomly selected as the control group. The remaining rats were injected with concanavalin A (ConA, 12.5 mg/kg) solution via tail vein to construct AIH model rat, which were randomly divided into AIH group, L-WG group (10 mg/kg), M-WG group (20 mg/kg), H-WG group (30 mg/kg), H-WG+VPA group (30 mg/kg WG+300 mg/kg Notch signal pathway activator VPA), 10 rats in each group and administered once a day for 10 days. Serum inflammatory factors and liver function indexes were detected by ELISA; HE staining was used to observe the pathological morphology of liver tissue; the level of spleen Th17/Treg cells was detected by flow cytometry; Western blot was used to detect the expression of spleen retinoid acid related orphan receptor γ t (RORγt), fork head box protein P3 (Foxp3) and liver Notch signal pathway proteins. Results The liver tissue structure of control group was normal and the staining was clear; In AIH group, the cells of liver tissue showed edema, the increase of cell volume led to the compression and narrowing of liver sinuses, and a large number of inflammatory cell infiltration and a small amount of necrosis occurred. The contents of alanine aminotransferase (ALT), aspartate aminotransferase (AST), interleukin (IL)-17 and IL-23, level of Th17 cells, Th17/Treg, the expression of RORγt, Notch, hes family bHLH transcription factor 1 gene (HES1) and hes related family bHLH transcription factor with YRPW motif 1 (HEY1) protein in AIH group were greatly higher than those in control group (P＜0.05), the contents of IL-10 and TNF-β, level of Treg cells, and level of Foxp3 protein were greatly lower(P＜0.05); Compared with AIH group, the liver injury in L-WG group, M-WG group and H-WG group was improved, the contents of ALT, AST, IL-17 and IL-23, level of Th17 cells, Th17/Treg, the expression of RORγt, Notch, HES1 and HEY1 protein were greatly lower (P＜0.05), the contents of IL-10 and TNF-β, level of Treg cells, and level of Foxp3 protein were greatly higher (P＜0.05); VPA reversed the improvement effect of H-WG on AIH rats. Conclusions WG could promote Th17/Treg cell balance in AIH rats by down-regulating Notch signal pathway. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Shenyang Pharmaceutical University is the property of Shenyang Pharmaceutical University and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Practical Pharmacy & Clinical Remedies is the property of Editorial Department of Practical Pharmacy & Clinical Remedies and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: Wogonin, a flavone identified in Scutellariae radix, shows in vitro and in vivo anti-cancer properties. However, the mechanism of action of wogonin on human gastric cancer (GC) cells remains unclear. Herein, this strudy was performed to investigate the influence of wogonin on cell migration and invasion in human GC cells MGC803 and its role in epithelial-mesenchymal transition (EMT). Methods: Effection on cell proliferation of human GC cells MGC803 was assessed by 3-(4,5)-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H-tetrazoliumbromide (MTT) assay. Wound-healing, transwell migration, and invasion assays were carried out to determine changes in MGC-803 cell migration and invasion. The influence of the wogonin on EMT was analyzed by both Western blotting and immunofluorescence. Results: Wogonin with the concentration of more than 20 μM effectively suppressed the proliferation of human GC MGC-803 cells. Different concentrations of wogonin inhibited the migration and invasion of human GC MGC-803 cells in a concentration- dependent manner. Furthermore, the application of wogonin resulted in the down-regulation of the mesenchymal biomarkers vimentin and ZEB1 but up-regulated the epithelial biomarker E-cadherin. Conclusion: Our findings indicate that wogonin imparts inhibitory effects on cell invasion and migration in GC, possibly by disrupting EMT. [ABSTRACT FROM AUTHOR]

Objective To investigate the combination inhibitory effect of the important components of baicalein and wogonin of suduxing, a new anti-hepatitis B virus (HBV) Chinese herbal on entecavir (ETV)-resistant mutant virus, and to find the optimal ratio of the two components. Methods The ETV-resistant HBV stable replication cell line HepG2. A64 was divided into the baicalein group, the wogonin group, the combined drug group, and the control group, respectively. According to the toxicity test results of baicalein and wogonin, cells in the the baicalein group were treated with baicalein at 4, 8, and 16 μ, mol/L, respectively, and recorded as the B4, B8, and B16 groups; cells in the wogonin group were treated with wogonin at 3, 6, and 12 μ, mol/L, respectively, and recorded as the W3, W6, and W12 groups. The first part of cells in the combined drug group was treated with baicalein (4 μ,mol/L) and the wogonin of different concentrations ( 3, 6, 12 μ,mol/L), respectively, and recorded as B4 + W3, B4 + W6, B4 + W12 groups ; the second part of cells in the combined drug group were treated with baicalein (8 μ,mol/L) and wogonin of different concentrations ( 3, 6, 12 μ, mol/L), recorded as B8 + W3, B8 + W6, B8 + W12 groups; the third part of cells in the combined drug group were treated with baicalein ( 16 μ,mol/L) and wogonin of different concentrations ( 3, 6, 12μ, mol/L), recorded as B16 + W3, B16 + W6, B16 + Wl2 groups. The cells in the control group were treated with an equal amount of DMEM medium. Cells of each group were cultured for 96 h, the HBV DNA in the cell supernatant was detected by the PCR-fluorescent probe "one-tube method", and the HBV DNA inhibition rate was calculated; the HBsAg in the cell supernatant was detected by the double antibody sandwich method, and the HBsAg inhibition rate was calculated; HBV total DNA and HBV covalently closed circular DNA ( cccDNA) were detected by fluorescence quantitative PCR method, and the inhibition rate of HBV total DNA and HBV cccDNA was calculated. The Q method of Jin Zhengjun was used to evaluate the synergism between baicalein and wogonin. Results The inhibition rates of HBV DNA, HBsAg in the cell supernatant, intracellular total DNA and cccDNA of the baicalein group, the wogonin group, and the combined drug group were higher than those in the control group ( all P < 0.05 ). The HBV DNA inhibition rate in the cell supernatant of the combined drug group was higher than that of each single drug ( all P <0.05), the B16 + W3 group had the highest Q value (0.970). The HBsAg inhibition rates in the cell supernatants of the B8 + W12, B16 + W3, and B16 + W12 groups were higher than that of each single group ( P < 0.05) The Q value of the B16 + W3 group was the highest (0.886). The inhibition rates of intracellular total HBV DNA of the combined drug group were higher than those of the baicalein group and wogonin group with the same drug concentration ( all P < 0.05) . The B16 + W3 group had the highest Q value ( 1.183). The inhibition rates of HBV cccDN A in the cells of B16 + W3, B16 + W6, and B16 + W12 groups were higher than those of the baicalein group and wogonin group with the same drug concentration, of which the B16 + W3 group had the highest Q value (0.972). Conclusions The baicalein and wogonin have inhibitory effects either individual or combination on ETV-resistant HBV DNA, HBV cccDNA, and HBsAg in HepG2. A64 cells. Inhibition effect of baicalein combined with wogonin is stronger than that of each single drug with the same drug concentration. The combination of 16μ, mol/L baicalein and 3μ, mol/L wogonin (5:1) has the optimal inhibitory effect. [ABSTRACT FROM AUTHOR]

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective： To investigate the effect of wogonin on proliferation and apoptosis of human osteosarcoma cell line 143 B and explore its possible mechanism. Methods： The human osteosarcoma cell line 143 B were cultured in vitro. CCK-8 assay was used to detected the anti-proliferation effect of different concentrations of wogonin on osteosarcoma 143 B cells. The effect of wogonin on cancer cell cycle distribution and apoptosis were analysis by flow cytometry. The expression level of Bax, Bcl-2, cleaved caspase-9 and cleaved caspase-3 were determined by western blot. Results： CCK-8 results showed that wogonin inhibited the proliferation of 143 B cells is a time-and concentration-dependent manners. Flow cytometry showed that wogonin could cause osteosarcoma cell cycle arrest in G0/G1 phase and induce apoptosis of osteosarcoma 143 B cells in a concentration dependent characteristic. Western Blot detection indicated that the expression of pro-apoptotic protein Bax was increased, and anti-apoptotic protein Bcl-2 wae decreased. Cleaved caspase-9 and cleaved caspase-3 were upregulated in osteosarcoma cells when treated with wogonin. Conclusion： Wogonin inhibited the proliferation of osteosarcoma cells, leading to cell cycle arrest, promoting cell apoptosis, and showed a time-and concentration-dependent manners,wogonin activated Caspase apoptosis pathway and induced cell cycle arrest may be the role of its mechanism of anti-osteosarcoma. [ABSTRACT FROM AUTHOR]

Objective To explore the effect of wogonin on the apoptosis of rheumatoid arthritis fibroblast-like synoviocytes ( ＲAFLS) and the associated molecular mechanisms． Methods FLSs were harvested from ＲA patients and cultured in joint synovial fluid and through 3-5 passages． With different treatments，cells were divided into six groups: control group，low-dose wogonin group ( 20 μg /mL of wogonin) ，middle-dose of wogonin group ( 50 μg /mL of wogonin) ，high-dose of wogonin group ( 100 μg / mL of wogonin) ，100 μg /mL Wogonin + NAC group，and 100 μg /mL Wogonin + SB203580 group． The proliferation of ＲA-FLS was measured with MTT assay． The apoptosis was measured with flow cytometric analysis． Mitochondrial membrane potential ( MMP) was measured with rhodamine 123 staining． The intracellular levels of reactive oxygen species ( ＲOS) were tested with DCFH-DA staining． The expression of proteins in p38 MAPK pathway was examined with Western blotting． Ｒesults Compared to the control group，different concentrations of wogonin inhibited ＲA-FLS growth，induced apoptosis，decreased mitochondrial membrane potential，and promoted p38MAPK phosphorylation and ＲOS production，and was in a concentration-dependent pattern． The apoptotic ratio of wogonin-treated group was markedly decreased by the ＲOS scavenger NAC or the p38MAPK inhibitor SB203580． and pretreatment of ＲA-FLS with 5 mmol /L NAC markedly reversed the wogonin-induced enhancement of p-p38 MAPK． Conclusion Wogonin effectively induces the apoptosis of FLS from rheumatoid arthritis patients through the induction of ＲOS formation and p38 MAPK activation． [ABSTRACT FROM AUTHOR]

Copyright of Practical Pharmacy & Clinical Remedies is the property of Editorial Department of Practical Pharmacy & Clinical Remedies and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Wogonin is a main effective component of Scutellaria baicalensis, with a significant anti-cancer activity. Recently, extensive studies focused on anti-cancer pharmacological effects of wogonin, but there were still a few studies on its molecular mechanism. Therefore, the molecular targets of its anti-cancer activity were still unclear. In this study, network pharmacology was applied to investigate the potential targets and molecular pathway of wogonin in inhibiting the growth of colorectal cancer. It indicated that Wnt/β-catenin was a key pathway of wogonin on colorectal cancer. Then, pharmacology and molecular mechanism studies were performed according to network pharmacological results. Pharmacological results revealed that wogonin inhibited significantly the proliferation of SW480(P<0.001), with a concentration-dependent regularity in the range of 12.5-50 μmol·L~(-1). Additionally, wogonin could induce G&#95;1 phase blocking of SW480 cells. Western blot was used to investigate the effect of wogonin on four characteristic proteins of Wnt/β-catenin pathway. CTNNB1(β-catenin), BIRC5(survivin) and GSK3 B were down-regulated significantly, while the expression level of BAX was up-regulated(P<0.05). In conclusion, wogonin could inhibit the proliferation of SW480 cells through Wnt/β-catenin pathway. The feature protein CTNNB1(β-catenin), BIRC5(survivin), GSK3 B and BAX were identified as the potential targets. This study illuminated the anti-cancer molecular mechanism and drug targets of wogonin, which provided a theoretical basis for anti-colon cancer drug discovery and clinical application.

This study investigated the inhibitory effect of eight natural flavonoids in Chinese herb Scutellariae Radix on huamn cytochrome P450 1 A(CYP1 A), a key cancer chemo-preventive target. In this study, phenacetin was used as a probe substrate for CYP1 A, while human liver microsomes and recombinant human CYP1 A enzymes were used as enzyme sources. Liquid chromatography-tandem mass spectrometry was used to monitor the formation rates of acetaminophen, the O-deethylated metabolite of phenacetin. The dose-dependent inhibition curves were depicted based on the changes of the formation rates of acetaminophen, while the IC&#95;(50) were determined. Inhibition kinetic analyses and docking simulations were used to investigate the inhibition modes and mechanism of wogonin(the most potent CYP1 A inhibitor in this herb), while the inhibition constants(K&#95;i) of wogonin against both CYP1 A1 and CYP1 A2 were determined. Among all tested flavonoids, wogonin, 7-methoxyflavanone and oroxylin A displayed a strong inhibitory effect on CYP1 A(IC&#95;(50)<1 μmol·L~(-1)), baicalein exhibited a moderate inhibitory effect on CYP1 A(IC&#95;(50) between 1-10 μmol·L~(-1)), and baicalin, scutellarein and wogonoside displayed a very weak inhibitory effect on CYP1 A(IC&#95;(50) between 10-25 μmol·L~(-1)), but scutellarin displayed a negligible inhibitory effect on CYP1 A(IC&#95;(50)>100 μmol·L~(-1)). Further investigations demonstrated that wogonin had a weak inhibitory effect on other human CYP enzymes, suggesting that it could be used as a lead compound for the development of specific inhibitors of CYP1 A. Furthermore, the inhibition kinetic analyses clearly demonstrated that wogonin could strongly inhibit phenacetin O-deethylation in both CYP1 A1 and CYP1 A2 in a competitive manner, with K&#95;i values at 0.118 and 0.262 μmol·L~(-1), respectively. Molecular docking demonstrated that wogonin could strongly interact with CYP1 A1 and CYP1 A2 via hydrophobic and π-π interactions, as well as Ser120 and Ser116 in CYP1 A1 via hydrogen-bonding. In conclusion, this study found that some flavonoids in Scutellariae Radix displayed a strong inhibitory effect on CYP1 A, while wogonin is the most potent CYP1 A inhibitor with a relatively high selectivity towards CYP1 A over other human CYPs.