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Fructus Zanthoxyli extract improves glycolipid metabolism disorder of type 2 diabetes mellitus via activation of AMPK/PI3K/Akt pathway:Network pharmacology and experimental validation

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Journal of Integrative Medicine 2022年第6期20卷 543-560页

作者： Ting Zhang Qing Zhang Wei Zheng Ting Tao Ruo-lan Li Li-yu Wang Wei Peng Chun-jie Wu School of Pharmacy Chengdu University of Traditional Chinese MedicineChengdu 611137Sichuan ProvinceChina

Objective:This study investigated the potential mechanisms behind the beneficial effects of Fructus Zanthoxyli(FZ)against type 2 diabetes mellitus(T2DM)based on Network pharmacology and experimental validation.Methods:Ultra-high-performance liquid chromatography coupled with hybrid quadrupole-orbitrap high-resolution mass spectrometry,and gas chromatography-mass spectrometry were used to identify the constituents of FZ.Next,the differentially expressed genes linked to the treatment of diabetes with FZ were screened using online databases(including Gene Expression Omnibus database and Swiss Target Prediction online database),and the overlapping genes and their enrichment were analyzed by Kyoto Encyclopedia of Genes and Genomes(KEGG).Finally,the pathway was verified by in vitro experiments,and cell staining with oil red and Nile red showed that the extract of FZ had a therapeutic effect on T2DM.Results:A total of 43 components were identified from FZ,and 39 differentially expressed overlapping genes were screened as the possible targets of FZ in T2DM.The dug component-target network indicated that PPARA,PPARG,PIK3R3,JAK2 and GPR88 might be the core genes targeted by FZ in the treatment of T2DM.Interestingly,the enrichment analysis of KEGG showed that effects of FZ against T2DM were closely correlated with the adenosine monophosphate-activated protein kinase(AMPK)and phosphatidylinositol-3-kinase(PI3K)/protein kinase B(Akt)signaling pathways.In vitro experiments further confirmed that FZ significantly inhibited palmitic acid-induced lipid formation in Hep G2 cells.Moreover,FZ treatment was able to promote the AMPK and PI3K/Akt expressions in Hep G2 cells.Conclusion:Network pharmacology combined with experimental validation revealed that FZ extract can improve the glycolipid metabolism disorder of T2DM via activation of the AMPK/PI3K/Akt pathway.

关键词： Fructus Zanthoxyli Zanthoxylum bungeanum Maxim Type 2 diabetes mellitus Network pharmacology Glucose and lipid metabolism Phosphatidylinositol-3-kinase AMPK/PI3K/Akt

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Network pharmacology and experimental validation to reveal the pharmacological mechanisms of Sini decoction(四逆汤)against renal fibrosis

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Journal of Traditional Chinese Medicine 2024年第2期44卷 362-372页

作者： WANG Yan DENG Fanying LIU Shiqi WANG Yingli Department of Pharmacy Shanxi University of Chinese MedicineJinzhong 030619China Schools of Basic Medical Sciences Heilongjiang University of Chinese MedicineHaerbin 150040China

OBJECTIVE:To investigate the mechanism by which Sini decoction(四逆汤,SND)improves renal fibrosis(Rf)in rats based on transforming growth factor β1/Smad(TGF-β1/Smad)signaling pathway.METHODS:Network pharmacology was applied to obtain potentially involved signaling pathways in SND's improving effects on Rf.The targets of SND drug components and the targets of Rf were obtained by searching databases,such as the Traditional Chinese Medicine Systems pharmacology Database and Analysis Platform(TCSMP)and GeenCard.The intersection targets of two searches were obtained and underwent signaling pathway analysis using a Venn diagram.Then experimental pharmacology was utilized to prove and investigate the effects of SND on target proteins in the TGF-β1/Smad signaling pathway.The Rf rat model was established by unilateral ureteral occlusion(UUO).The expression levels of transforming growth factor,matrix metalloproteinase-9(MMP-9),matrix metal protease-2(MMP-2),connective tissue growth factor(CTGF),and tissue inhibitor of metalloproteinase-1(TIMP-1)were determined by Masson staining of rat renal tissue,and immunohistochemical methods.The expression levels of Smad3,Smad2,and Smad7 in renal tissue were determined by Western blotting(WB).The mechanism of the improving effects of SND on Rf was investigated based on TGF-β1/Smad signaling pathway.RESULTS:A total of 12 drug components of Fuzi(Radix Aconiti Lateralis Preparata),5 drug components of Ganjiang(Rhizoma Zingiber),and 9 drug components of Gancao(Radix Glycy et Rhizoma)were obtained from the database search,and 207 shared targets were found.A total of 1063 Rf targets were found in the database search.According to the Venn diagram,in total,96 intersection targets were found in two database searches.The metabolic pathways involved included TGF-β signaling pathway,phosphatidylinositol-3-kinase/serine-threonine protein kinase signaling(PI3K/Akt)pathway,and hypoxia-inducible factor-1(HIF-1)signaling pathway.Masson staining analysis showed that compared with the model group,the renal

关键词： renal fibrosis Network pharmacology transforming growth factor beta1 smad proteins Sini decoction

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Rheum palmatum L. and Salvia miltiorrhiza Bge. Alleviates Acute Pancreatitis by Regulating Th17 Cell Differentiation: An Integrated Network pharmacology Analysis, Molecular Dynamics Simulation and Experimental Validation

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Chinese Journal of Integrative Medicine 2024年第5期30卷 408-420页

作者： FENG Min-chao LUO Fang HUANG Liang-jiang LI Kai CHEN Zu-min LI Hui YAO Chun QIN Bai-jun CHEN Guo-zhong The First Clinical Medical College Guangxi University of Traditional Chinese MedicineNanning 530000China Guangxi Key Laboratory of Molecular Biology of Traditional Chinese Medicine and Preventive Medicine Nanning 530000China Graduate School Guangxi University of Traditional Chinese MedicineNanning 530000China Department of Gastroenterology the First Affiliated Hospital of Guangxi University of Traditional Chinese MedicineNanning 530023China

Objective: To identify the core targets of Rheum palmatum L. and Salvia miltiorrhiza Bge.,(Dahuang-Danshen, DH-DS) and the mechanism underlying its therapeutic efficacy in acute pancreatitis(AP)using a Network pharmacology approach and validate the findings in animal experiments. Methods: Network pharmacology analysis was used to elucidate the mechanisms underlying the therapeutic effects of DH-DS in AP. The reliability of the results was verified by molecular docking simulation and molecular dynamics simulation.Finally, the results of Network pharmacology enrichment analysis were verified by immunohistochemistry,Western blot analysis and real-time quantitative PCR, respectively. Results: Sixty-seven common targets of DH-DS in AP were identified and mitogen-activated protein kinase 3(MAPK3), Janus kinase 2(JAK2), signal transducer and activator of transcription 3(STAT3), protein c-Fos(FOS) were identified as core targets in the protein interaction(PPI) network analysis. Gene ontology analysis showed that cellular response to organic substance was the main functions of DH-DS in AP, and Kyoto Encyclopedia of Genes and Genomes analysis showed that the main pathway included Th17 cell differentiation. Molecular docking simulation confirmed that DH-DS binds with strong affinity to MAPK3, STAT3 and FOS. Molecular dynamics simulation revealed that FOS-isotanshinone Ⅱ and STAT3-dan-shexinkum d had good binding capacity. Animal experiments indicated that compared with the AP model group, DH-DS treatment effectively alleviated AP by inhibiting the expression of interleukin-1β, interleukin-6 and tumor necrosis factor-α, and blocking the activation of Th17 cell differentiation(P<0.01). Conclusion: DH-DS could inhibit the expression of inflammatory factors and protect pancreatic tissues,which would be functioned by regulating Th17 cell differentiation-related m RNA and protein expressions.

关键词： Rheum palmatum L. Salvia miltiorrhiza Bge. molecular docking simulation Network pharmacology acute pancreatitis Th17 cell differentiation

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Network pharmacology and in vitro Experimental Veriflcation on Intervention of Quercetin, Present in Chinese Medicine Yishen Qutong Granules, on Esophageal Cancer

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Chinese Journal of Integrative Medicine 2023年第3期29卷 233-243页

作者： LI Jie CHANG Jin-yuan JIANG Zheng-long YIN Yu-kun CHEN Jia-yang JIN Wei LI Hao FENG Li National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing(100021)China Dongzhimen Hospital Beijing University of Chinese MedicineBeijing(100029)China

Objective: To explore the potential mechanism of Yishen Qutong Granules(YSQTG) for the treatment of esophageal cancer using Network pharmacology and experimental research. Methods: The effective components and molecular mechanism of YSQTG in treating esophageal cancer were expounded based on Network pharmacology and molecular docking. The key compound was identified by high-performance liquid chromatography and mass spectrometry(HPLC-MS) to verify the malignant phenotype of the key compounds in the treatment of esophageal cancer. Then, the interaction proteins of key compounds were screened by pull-down assay combined with mass spectrometry. RNA-seq was used to screen the differential genes in the treatment of esophageal cancer by key compounds, and the potential mechanism of key compounds on the main therapeutic targets was verified. Results: Totally 76 effective compounds of YSQTG were found, as well as 309 related targets, and 102 drug and disease interaction targets. The drug-compound-target network of YSQTG was constructed, suggesting that quercetin, luteolin, wogonin, kaempferol and baicalein may be the most important compounds, while quercetin had higher degree value and degree centrality, which might be the key compound in YSQTG. The HPLC-MS results also showed the stable presence of quercetin in YSQTG. By establishing a protein interaction network, the main therapeutic targets of YSQTG in treating esophageal cancer were Jun proto-oncogene, interleukin-6, tumor necrosis factor, and RELA proto-oncogene. The results of cell function experiments in vitro showed that quercetin could inhibit proliferation, invasion, and clonal formation of esophageal carcinoma cells. Quercetin mainly affected the biological processes of esophageal cancer cells, such as proliferation, cell cycle, and cell metastasis. A total of 357 quercetin interacting proteins were screened, and 531 genes were significantly changed. Further pathway enrichment analysis showed that quercetin mainly affects the metabolic pathway, MAPK signaling

关键词： Network pharmacology esophageal cancer Yishen Qutong Granule Chinese medicine quercetin nuclear factor kappa B

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Eight Zhes Decoction ameliorates the lipid dysfunction of nonalcoholic fatty liver disease using integrated lipidomics, Network pharmacology and pharmacokinetics

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Journal of Pharmaceutical Analysis 2023年第9期13卷 1058-1069页

作者： Yuping Zhou Ze Dai Kaili Deng Yubin Wang Jiamin Ying Donghui Chu Jinyue Zhou Chunlan Tang The First Affiliated Hospital of Ningbo University NingboZhejiang315020China School of Public Health Health Science CenterNingbo UniversityNingboZhejiang315211China Institute of Digestive Disease of Ningbo University NingboZhejiang315020China

Nonalcoholic fatty liver disease(NAFLD)has developed into the most common chronic liver disease and can lead to liver cancer.Our laboratory previously developed a novel prescription for NAFLD,“Eight Zhes Decoction”(EZD),which has shown good curative effects in clinical practice.However,the pharmacodynamic material basis and mechanism have not yet been revealed.A strategy integrating lipidomics,Network pharmacology and pharmacokinetics was used to reveal the active components and mechanisms of EZD against NAFLD.The histopathological results showed that EZD attenuated the degrees of collagen deposition and steatosis in the livers of nonalcoholic steatofibrosis model mice.Furthermore,glycerophospholipid metabolism,arachidonic acid metabolism,glycerolipid metabolism and linoleic acid metabolism with phospholipase A2 group IVA(PLA2G4A)and cytochrome P450 as the core targets and 12,13-cis-epoxyoctadecenoic acid,12(S)-hydroxyeicosatetraenoic acid,leukotriene B4,prostaglandin E2,phosphatidylcholines(PCs)and triacylglycerols(TGs)as the main lipids were found to be involved in the treatment of NAFLD by EZD.Importantly,naringenin,artemetin,canadine,and bicuculline were identified as the active ingredients of EZD against NAFLD;in particular,naringenin reduces PC consumption by inhibiting the expression of PLA2G4A and thus promotes sufficient synthesis of very-low-density lipoprotein to transport excess TGs in the liver.This research provides valuable data and theoretical support for the application of EZD against NAFLD.

关键词： Eight Zhes Decoction Nonalcoholic fatty liver disease Lipidomics Network pharmacology Pharmacokinetics

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A Network pharmacology-Based Study on Antidepressant Effect of Salicornia europaea L.Extract with Experimental Support in Chronic Unpredictable Mild Stress Model Mice

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Chinese Journal of Integrative Medicine 2022年第4期28卷 339-348页

作者： SUN Dan-chen WANG Ran-ran XU Hao ZHU Xue-hui SUN Yan QIAO Shi-qing QIAO Wei Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics School of PharmacyTianjin Medical UniversityTianjin300070China

Objective:To investigate the pharmacodynamic material basis,mechanism of actions and targeted diseases of Salicornia europaea L.(SE)based on the Network pharmacology method,and to verify the antidepressant-like effect of the SE extract by pharmacological experiments.Methods:Retrieval tools including Chinese medicine(CM),PubMed,PharmMapper,MAS 3.0 and Cytoscape were used to search the components of SE,predict its targets and related therapeutic diseases,and construct the"Component-TargetPathway"network of SE for central nervous system(CNS)diseases.Further,protein-protein interaction(PPI)network,Kyoto Encyclopedia of Genes and Genomes(KEGG)and Gene Ontology(GO)function annotation of depression-related targets were analyzed to predict the antidepressant mechanism of SE.Chronic unpredictable mild stress(CUMS)model was used to construct a mouse model with depression-like symptoms.And the animals were randomly divided into 6 groups(n=10)including the normal group(nonstressed mice administered with distilled water),the CUMS group(CUMS mice administered with distilled water),the venlafaxine group(CUMS mice administered with venlafaxine 9.38 mg/kg),SE high-,medium-,and low-dose groups(CUMS mice administered with SE 1.8,1.35 and 0.9 g/kg,respectively).Then some relevant indicators were determined for experimental verification by the forced swim test(FST),the tail suspension test(TST)and open-field test(OFT).Dopamine(DA)concentration in hippocampus and cerebral cortex,IL-2 and corticosterone(CORT)levels in blood,and nuclear factor E2 related factor 2(Nrf2),kelch-like epichlorohydrin related protein 1(Keap1),NAD(P)H dehydrogenase[quinone]1(NQO1)and heme oxygenase-1(HO-1)levels in mice were measured by enzyme linked immunosorbent assay(ELISA)and Western blot respectively to explore the possible mechanisms.Results:The"target-disease"network diagram predicted by Network pharmacology,showed that the potential target of SE involves a variety of CNS diseases,among which depression accounts for the majority.The experimental results

关键词： Salicornia europaea L. Network pharmacology tail suspension test forced swim test depression

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Exploring the mechanism of hirudin in the treatment of diabetic kidney disease using Network pharmacology combined with molecular docking verification

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Journal of Traditional Chinese Medicine 2022年第4期42卷 586-594页

作者： PANG Xinxin ZHU Qing PENG Zining ZHANG Yage SHI Xiujie HAN Jiarui Department of Nephropathy Henan Provincial Hospital of Traditional Chinese MedicineZhengzhou 450002China

OBJECTIVE:To explore the mechanism of hirudin in the treatment of diabetic kidney disease(DKD).METHOD:Cytoscape software was used to analyze the network between hirudin targets and active components in the treatment of DKD.The biological function and mechanism of effective targets of hirudin for DKD treatment were analyzed by the Database for Annotation,Visualization and Integrated Discovery(DAVID)database.Molecular docking technology was used to simulate the docking of key targets,and the DKD rat model was used to verify the first 4 key targets with high"Hydrogen number"among the top 10 targets verified by molecular docking.RESULTS:Total of 12334 DKD targets were screened in Gene Cards,OMIM and other databases,Hirudin and DKD had 247 common target genes,and the protein interaction network got 2115 edges.The DAVID database was used for the Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis,confirming that hirudin in treatment of DKD involves multiple signaling pathways such as the forkhead box O signaling pathway,the phosphatidylinositol 3-kinase-protein kinase B signaling pathway,the vascular endothelial-derived growth factor signaling pathway and other signaling pathways.The top ten key targets of hirudin in treatment of DKD were verified by molecular docking.Animal experiments showed that hirudin could decrease the expression of caspase-3 in renal tissue of DKD rats,and increase the expression of RAC-alpha serine/threonineprotein kinase,Catalase,and Heat shock protein HSP 90-alpha in renal tissue of DKD rats.CONCLUSION:This study preliminarily reveals that hirudin treats DKD through multiple targets and pathways,and molecular docking and animal experiments indicates the feasibility of this study.Hirudin may be directly or indirectly involved in the regulation of cell metabolism,oxidative stress and other mechanisms in the treatment of DKD,which will lay the foundation for future molecular biological experiments of hirudin in the treatment of DKD.

关键词： hirudins diabetic kidney disease Network pharmacology molecular docking simulation

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Therapeutic Mechanism of Kai Xin San on Alzheimer's Disease Based on Network pharmacology and Experimental Validation

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Chinese Journal of Integrative Medicine 2023年第5期29卷 413-423页

作者： WANG Kan YANG Rong CHEN Tuan-tuan QIN Mei-rong WANG Ping KONG Ming-wang The Second Clinical Medical College Guangzhou University of Chinese MedicineGuangzhou(510006)China Department of Hepatology Shenzhen Traditional Chinese Medicine HospitalThe Fourth Clinical Medical College of Guangzhou University of Chinese MedicineShenzhenGuangdong Province(518033)China Faculty of Chinese Medicine and State Key Laboratory of Quality Research in Chinese Medicine Macao University of Science and TechnologyMacao SARChina Key Laboratory of Cosmetics Monitoring and Evaluation State Drug AdministrationShenzhen Institute for Drug ControlShenzhenGuangdong Province(518057)China The School of Basic Medical Sciences Hubei University of Chinese MedicineWuhan(430065)China

Objective: To explore the specific pharmacological molecular mechanisms of Kai Xin San(KXS)on treating Alzheimer’s disease(AD) based on Network pharmacology and experimental validation. Methods:The chemical compounds of KXS and their corresponding targets were screened using the Encyclopedia of Traditional Chinese Medicine(ETCM) database. AD-related target proteins were obtained from MalaCards database and DisGeNET databases. Key compounds and targets were identified from the compound-targetdisease network and protein-protein interaction(PPI) network analysis. Functional enrichment analysis predicted the potential key signaling pathways involved in the treatment of AD with KXS. The binding affinities between key ingredients and targets were further verified using molecular docking. Finally, the predicted key signaling pathway was validated experimentally. Positioning navigation and space search experiments were conducted to evaluate the cognitive improvement effect of KXS on AD rats. Western blot was used to further examine and investigate the expression of the key target proteins related to the predicted pathway. Results: In total, 38active compounds and 469 corresponding targets of KXS were screened, and 264 target proteins associated with AD were identified. The compound-target-disease and PPI networks identified key active ingredients and protein targets. Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway analysis suggested a potential effect of KXS in the treatment of AD via the amyloid beta(Aβ)-glycogen synthase kinase-3 beta(GSK3β)-Tau pathway. Molecular docking revealed a high binding affinity between the key ingredients and targets. In vivo,KXS treatment significantly improved cognitive deficits in AD rats induced by Aβ1-42, decreased the levels of Aβ, p-GSK3β, p-Tau and cyclin-dependent kinase 5, and increased the expressions of protein phosphatase 1alpha(PP1A) and PP2A(P<0.05 or P<0.01). Conclusion: KXS exerted neuroprotective effects by regulating the Aβ-GSK3β-Tau signaling pathway, which provides

关键词： Kai Xin San Alzheimer's disease Tau protein Network pharmacology molecular docking experimental validation Chinese medicine

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Network pharmacology and molecular docking study on the effect of Kaempferol in treatment of metabolic associated fatty liver disease

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Journal of Traditional Chinese Medicine 2022年第5期42卷 788-794页

作者： ZHOU Kaixuan ZHANG Dong BAO Huiwei LI Lijing College of Pharmacy Changchun University of Chinese MedicineChangchun 130117China

OBJECTIVE: To study therapeutic effect of kaempferol on metabolic associated fatty liver disease(MAFLD) by Network pharmacology and molecular docking combined with cell experiments. METHODS: First, use the Swiss Target Prediction database to predict the targets of kaempferol, and collect the targets of MAFLD through the Disgenet database and the Gene Cards database. Then, the common target of kaempferol and MAFLD was enriched and analyzed by the Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes, and the protein-protein interaction(PPI) network was constructed through the string database to obtain the key targets, and carry out molecular docking of key targets with kaempferol;In cell experiment, oleic acid induced steatosis in Hep G2 cells, which was intervened by kaempferol, the level of triglyceride(TG) was detected, the lipid deposition was observed by oil red O staining, and the protein expression was detected by Western blot. RESULTS: The results showed that there are 33 common targets for kaempferol and MAFLD. The biological process of GO is related to the regulation of protein kinase B, cell apoptosis, inflammatory factors, lipoxygenase, etc. Its action pathway is related to the phosphatidylinositol-3-kinase and protein kinase B(PI3K-AKT) signaling pathway, hypoxia-inducible factor 1 signaling pathway, forkhead box protein O signaling pathway, AMP-activated protein kinase signaling pathway, tumor necrosis factor signaling pathway, etc., the key targets are protein kinase B(AKT1), prostaglandin G/H synthase 2, matrix metalloproteinase-9, epidermal growth factor receptor, and the molecular docking of kaempferol with the four key targets shows good binding properties. Cell experiments show that kaempferol can reduce cell TG levels, reduce lipid deposition, increase the expression of PI3K, AKT, and beclin-1, and reduce the expression of caspase-3 and nuclear factor-kappa B. Kaempferol can treat MAFLD by regulating the PI3K-AKT signaling pathway to regulate cell autophagy, apoptosis, and inflammation

关键词： Metabolic associated fatty liver disease kaempferol Network pharmacology molecular docking simulation protein kinase B protoonco-gene proteins c-akt signaling transduction

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Mechanism of Huashi Xingyu Qingre recipe(化湿行淤清热方)in treating oral lichen planus based on Network pharmacology and clinical trial verification

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Journal of Traditional Chinese Medicine 2022年第2期42卷 304-313页

作者： DENG Qianlan LU Yueting YAN Lijuan LU Hualin JIN Ruizhe XU Yanzhi SONG Jing LIU Tiejun Department of Stomatology the Fourth Hospital of Hebei Medical UniversityShijiazhuang 050000China Department of Stomatology Hebei Children's HospitalShijiazhuang 050000China Department of Stomatology Shijiazhuang Third HospitalShijiazhuang 050000China

OBJECTIVE:To identify the main active components and targets of Huashi Xingyu Qingre recipe(化湿行淤清热方,HXQR)and to investigate its mechanism in the treatment of oral lichen planus(OLP).METHODS:The Traditional Chinese Medicine Systems pharmacology Database and Analysis Platform was searched to identify the active ingredients and corresponding targets of HXQR.Disease genes were obtained from the Gene Cards database,and a“drugdisease regulatory network”was constructed using Cytoscape software and PERL programming language.The STRING database was used to build a protein-protein interaction network.Gene ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)terms were analyzed using R software with a Bioconducter plugin.Finally,the results and the efficacy of HXQR in treating OLP were validated in a clinical trial that included enzyme-linked immunosorbent assay(ELISA)testing and observations of the post-treatment changes in clinical symptoms.RESULTS:HXQR contained 167 active components and 261 targets,with 391 disease targets.The intersection of these two categories in a Venn diagram revealed 57 drugdisease common targets.A compound-target network was constructed and revealed that the six key pharmaceutical ingredients of HXQR were quercetin,luteolin,wogonin,kaempferol,beta-carotene,and baicalein.The protein-protein interaction network mainly involved core proteins such as ALB,interleukin-6,and AKT1.Drug-disease common targets were enriched in 1628 GO terms and 117 KEGG terms,mainly involving inflammatory responses,viral infections,and tumorrelated pathways.ELISA testing indicated that HXQR inhibited the tumor necrosis factor(TNF)signaling pathway by reducing the expression of interleukin-6,matrix metalloproteinase-9,and intercellular adhesion molecule-1.The clinical symptoms of the patients with OLP were significantly improved after 8 weeks of treatment with HXQR.CONCLUSION:HXQR treats OLP by regulating the TNF signaling pathway,resulting in a marked treatment effect with few adverse effects.

关键词： lichen planus oral Network pharmacology clinical trial Huashi Xingyu Qingre recipe

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