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Article: Analyzing the potential therapeutic mechanism of Huashi Baidu Decoction on severe COVID-19 through integrating network pharmacological methods.

Zhu, Yi-Wei / Yan, Xiao-Feng / Ye, Ting-Jie / Hu, Jing / Wang, Xiao-Ling / Qiu, Feng-Jun / Liu, Cheng-Hai / Hu, Xu-Dong

Journal of traditional and complementary medicine

2021 Volume 11, Issue 2, Page(s) 180–187

Abstract: Background and aim: Huashi Baidu Decoction (HSBD) is a novel complex prescription which has positive effects on severe COVID-19. This study was aimed to discover key Chinese materia medica, main active compounds, hub therapeutic target proteins and core ...

Abstract	Background and aim: Huashi Baidu Decoction (HSBD) is a novel complex prescription which has positive effects on severe COVID-19. This study was aimed to discover key Chinese materia medica, main active compounds, hub therapeutic target proteins and core signal pathways in the potential therapeutic mechanism of HSBD on severe COVID-19 through integrating network pharmacological methods. Experimental procedure: TCMSP, TCMID and STITCH databases were used to screen out active compounds and target proteins of HSBD. GeneCards database was used to screen out disease genes of severe COVID-19. The potential therapeutic targets of HSBD on severe COVID-19 were used to construct protein-protein interaction network through STRING database and the hub target proteins were discovered. Next, GO and KEGG enrichment analysis were carried out to discover core signal pathways. Finally, the network diagram of "Chinese materia medica-active compounds-therapeutic target proteins" was built, then key Chinese materia medica and main active compounds were selected. Results and conclusion: HSBD might treat severe COVID-19 through 45 potential target genes, among them, there were 13 hub target genes: RELA, TNF, IL6, IL1B, MAPK14, TP53, CXCL8, MAPK3, MAPK1, IL4, MAPK8, CASP8, STAT1. Meanswhile, GO_BiologicalProcess and KEGG signaling pathways analysis results showed that the core signal pathways were inflammation and immune regulation pathways. Finally, 4 key Chinese materia medica and 11 main active compounds were discovered in the HSBD. In conclusion, the therapeutic mechanism of HSBD on severe COVID-19 might involve its pharmacological effects of anti-inflammation and immune regulation via acting on 45 disease-related proteins of severe COVID-19. Taxonomy classification by evise: Viral Pneumonia, COVID-19, Acute Respiratory Distress Syndrome, Septic Shock, Chinese Herbal Medicine.
Language	English
Publishing date	2021-01-18
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2709698-1
ISSN	2225-4110
ISSN	2225-4110
DOI	10.1016/j.jtcme.2021.01.004
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Article ; Online: High mobility group box-1 release from H

Ye, Ting-Jie / Lu, Yan-Lin / Yan, Xiao-Feng / Hu, Xu-Dong / Wang, Xiao-Ling

World journal of gastroenterology

2019 Volume 25, Issue 36, Page(s) 5434–5450

Abstract: Background: High mobility group box-1 (HMGB1), recognized as a representative of damage-associated molecular patterns, is released during cell injury/death, triggering the inflammatory response and ultimately resulting in tissue damage. Dozens of ... ...

Abstract	Background: High mobility group box-1 (HMGB1), recognized as a representative of damage-associated molecular patterns, is released during cell injury/death, triggering the inflammatory response and ultimately resulting in tissue damage. Dozens of studies have shown that HMGB1 is involved in certain diseases, but the details on how injured hepatocytes release HMGB1 need to be elicited. Aim: To reveal HMGB1 release mechanism in hepatocytes undergoing oxidative stress. Methods: C57BL6/J male mice were fed a high-fat diet for 12 wk plus a single binge of ethanol to induce severe steatohepatitis. Hepatocytes treated with H Results: When hepatocytes were damaged, HMGB1 translocated from the nucleus to the cytoplasm because of its hyperacetylation and was passively released outside both in vivo and in vitro. After treatment with Sirt1-siRNA or Sirt1 inhibitor (EX527), the hyperacetylated HMGB1 in hepatocytes increased, and Sirt1 activity inhibited by H Conclusion: The functional inhibition between Parp1 and Sirt1 leads to HMGB1 hyperacetylation, which leads to its translocation from the nucleus to the cytoplasm and finally outside the cell.
MeSH term(s)	Acetylation/drug effects ; Animals ; Carbazoles/pharmacology ; Cell Line ; Cell Nucleus/metabolism ; Cells, Cultured ; Cytoplasm/metabolism ; Diet, High-Fat/adverse effects ; Disease Models, Animal ; Ethanol/toxicity ; Fatty Liver/diagnosis ; Fatty Liver/etiology ; Fatty Liver/pathology ; HMGB1 Protein/metabolism ; Hepatocytes/cytology ; Hepatocytes/pathology ; Humans ; Hydrogen Peroxide/toxicity ; Liver/cytology ; Liver/drug effects ; Liver/pathology ; Liver Function Tests ; Male ; Mice ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Poly (ADP-Ribose) Polymerase-1/antagonists & inhibitors ; Poly (ADP-Ribose) Polymerase-1/metabolism ; Quinolinium Compounds/pharmacology ; RNA, Small Interfering/metabolism ; Sirtuin 1/antagonists & inhibitors ; Sirtuin 1/genetics ; Sirtuin 1/metabolism
Chemical Substances	4-(4-(dihexadecylamino)styryl)-N-methylquinolinium iodide ; 6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide ; Carbazoles ; HMGB1 Protein ; HMGB1 protein, mouse ; Quinolinium Compounds ; RNA, Small Interfering ; Ethanol (3K9958V90M) ; Hydrogen Peroxide (BBX060AN9V) ; Parp1 protein, mouse (EC 2.4.2.30) ; Poly (ADP-Ribose) Polymerase-1 (EC 2.4.2.30) ; Sirt1 protein, mouse (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2019-09-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	2185929-2
ISSN	2219-2840 ; 1007-9327
ISSN (online)	2219-2840
ISSN	1007-9327
DOI	10.3748/wjg.v25.i36.5434
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Article: The Study of Yin-Chen-Hao-Tang Preventing and Treating Alcoholic Fatty Liver Disease through PPAR Signaling Pathway Based on Network Pharmacology and RNA-Seq Transcriptomics.

Zhu, Yi-Wei / Li, Du / Ye, Ting-Jie / Qiu, Feng-Jun / Wang, Xiao-Ling / Yan, Xiao-Feng / Lu, Yan-Lin / Xu, Wei / Li, Hua / Hu, Xu-Dong

Evidence-based complementary and alternative medicine : eCAM

2021 Volume 2021, Page(s) 8917993

Abstract: Background: Alcoholic fatty liver disease (AFLD) is the first stage of the alcoholic liver disease course. Yin-Chen-Hao-Tang (YCHT) has a good clinical effect on the treatment of AFLD, but its molecular mechanism has not been elucidated. In this study, ... ...

Abstract	Background: Alcoholic fatty liver disease (AFLD) is the first stage of the alcoholic liver disease course. Yin-Chen-Hao-Tang (YCHT) has a good clinical effect on the treatment of AFLD, but its molecular mechanism has not been elucidated. In this study, we tried to explore the molecular mechanism of YCHT in improving hepatocyte steatosis in AFLD mice through network pharmacology and RNA sequencing (RNA-Seq) transcriptomics. Methods: Network pharmacological methods were used to analyze the potential therapeutic signaling pathways and targets of YCHT on AFLD. Then, the AFLD mice model was induced and YCHT was administered concurrently. Liver injury was measured by serum alanine aminotransferase (ALT) activity and liver tissue H&E staining, and liver steatosis was determined by serum triglyceride (TG) level and liver tissue Oil Red staining. The molecular mechanism of YCHT on prevention and treatment of mice AFLD was investigated according to the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of the differential expression genes data obtained by liver tissue RNA-Seq. Finally, ethanol-induced AFLD AML12 hepatocyte model was established, YCHT with or without PPAR Results: The results of network pharmacology analysis showed that YCHT may exert its pharmacological effect on AFLD through 312 potential targets which are involved in many signaling pathways including the PPAR signaling pathway. AFLD mice experiments results showed that YCHT markedly decreased mice serum ALT activity and serum TG levels. YCHT also significantly improved alcohol-induced hepatic injury and steatosis in mice livers. Furthermore, KEGG pathway enrichment results of RNA-Seq showed that the PPAR signaling pathway should be the most relevant pathway of YCHT in the prevention and treatment of AFLD. AFLD hepatocyte model experiment results showed that YCHT could remarkably reduce hepatocyte steatosis through reducing PPAR Conclusions: Our study discovered that PPAR
Language	English
Publishing date	2021-12-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	2171158-6
ISSN	1741-4288 ; 1741-427X
ISSN (online)	1741-4288
ISSN	1741-427X
DOI	10.1155/2021/8917993
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Article ; Online: Adipose-Specific Lipin-1 Overexpression Renders Hepatic Ferroptosis and Exacerbates Alcoholic Steatohepatitis in Mice.

Zhou, Zhou / Ye, Ting Jie / Bonavita, Gregory / Daniels, Michael / Kainrad, Noah / Jogasuria, Alvin / You, Min

Hepatology communications

2019 Volume 3, Issue 5, Page(s) 656–669

Abstract: Lipin-1 is a ... ...

Abstract	Lipin-1 is a Mg
Language	English
Publishing date	2019-03-12
Publishing country	United States
Document type	Journal Article
ISSN	2471-254X
ISSN (online)	2471-254X
DOI	10.1002/hep4.1333
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Article ; Online: Intestinal SIRT1 Deficiency Protects Mice from Ethanol-Induced Liver Injury by Mitigating Ferroptosis.

Zhou, Zhou / Ye, Ting Jie / DeCaro, Elizabeth / Buehler, Brian / Stahl, Zachary / Bonavita, Gregory / Daniels, Michael / You, Min

The American journal of pathology

2019 Volume 190, Issue 1, Page(s) 82–92

Abstract: Aberrant liver sirtuin 1 (SIRT1), a mammalian ... ...

Abstract	Aberrant liver sirtuin 1 (SIRT1), a mammalian NAD
MeSH term(s)	Animals ; Anti-Infective Agents, Local/toxicity ; Chemical and Drug Induced Liver Injury/etiology ; Chemical and Drug Induced Liver Injury/metabolism ; Chemical and Drug Induced Liver Injury/prevention & control ; Disease Models, Animal ; Ethanol/toxicity ; Female ; Ferroptosis ; Inflammation/etiology ; Inflammation/metabolism ; Inflammation/prevention & control ; Intestines/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Oxidative Stress ; Protective Agents ; Signal Transduction ; Sirtuin 1/physiology
Chemical Substances	Anti-Infective Agents, Local ; Protective Agents ; Ethanol (3K9958V90M) ; Sirt1 protein, mouse (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2019-10-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2019.09.012
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Article ; Online: Total extract of Xin Jia Xuan Bai Cheng Qi decoction inhibits pulmonary fibrosis via the TGF-β/Smad signaling pathways in vivo and in vitro.

Qin, Hui / Wen, Hao-Tian / Gu, Kai-Juan / Hu, Xu-Dong / Yang, Tao / Yan, Xiao-Feng / Ye, Ting-Jie / Huo, Jin-Lin / Hu, Jing

Drug design, development and therapy

2019 Volume 13, Page(s) 2873–2886

Abstract: Purpose: Pulmonary fibrosis (PF) is a common clinical disease, which results in serious respiratory impairment. Xin Jia Xuan Bai Cheng Qi Decoction (XJXBCQ) is a traditional prescription commonly used in treating lung diseases. We investigate the effect ...

Abstract	Purpose: Pulmonary fibrosis (PF) is a common clinical disease, which results in serious respiratory impairment. Xin Jia Xuan Bai Cheng Qi Decoction (XJXBCQ) is a traditional prescription commonly used in treating lung diseases. We investigate the effect of XJXBCQ against PF and its mechanism via the regulation of TGF-β1/Smad in vitro and in vivo. Materials and methods: XJXBCQ was first extracted and probed for chemical characterization. An PF model in vitro and in vivo was established in rats and in MRC-5 cells. In bleomycin (BLM)-induced rats model, lung function such as peak expiratory flow (PEF), minute ventilation (MV) and hydroxyproline (HYP) were measured; histopathological changes of lung tissue and TGF-β1 in peripheral blood of rats were detected. TGF-β receptor, Smad2 and its phosphorylation expression were tested by Western blot assay in rats model. Then the effects of XJXBCQ on TGF-β1/Smad signal pathway were assessed by Western blot analysis in vitro, and IL-17A and IL-25 levels were evaluated by ELISA in vivo. Results: Our results showed that XJXBCQ significantly enhanced the lung functions, such as PEF, MV and HYP, by reducing the expression level of lung inflammatory cytokine and the content and fibrosis of lung collagen. Moreover, XJXBCQ effectively inhibited TGF-β1, Smad2 and its phosphorylation expression, and the activation of Smad7 in vitro and in vivo. Furthermore, XJXBCQ had an inhibitory effect on the α-smooth muscle actin (α-SMA) and fibronectin (Fn) in vitro and downregulated IL-17A and IL-25 by inhibiting the activation of TGF-β1/Smad signaling pathway in vitro and in vivo. Further, XJXBCQ effectively inhibitied ventilation volume and peak expiratory content remodeling and hydroxyproline content through inhibition of TGF-βRⅡ, Smad2 and its phosphorylation expression, and activation of Smad7 in vivo. Conclusion: XJXBCQ extract had an anti-PF effect in vitro and in vivo, which could be attributed to the inhibition of the expression of p-Smad2 and increase in the expression of Smad7 by regulating the TGF-β1/Smad activity.
MeSH term(s)	Animals ; Cells, Cultured ; Cytokines/metabolism ; Disease Models, Animal ; Drugs, Chinese Herbal/pharmacology ; Humans ; Male ; Plant Extracts/pharmacology ; Pulmonary Fibrosis/drug therapy ; Pulmonary Fibrosis/physiopathology ; Rats ; Rats, Wistar ; Receptors, Transforming Growth Factor beta/metabolism ; Signal Transduction/drug effects ; Smad2 Protein/metabolism ; Smad7 Protein/metabolism ; Transforming Growth Factor beta1/metabolism
Chemical Substances	Cytokines ; Drugs, Chinese Herbal ; Plant Extracts ; Receptors, Transforming Growth Factor beta ; Smad2 Protein ; Smad7 Protein ; Transforming Growth Factor beta1
Language	English
Publishing date	2019-08-19
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2451346-5
ISSN	1177-8881 ; 1177-8881
ISSN (online)	1177-8881
ISSN	1177-8881
DOI	10.2147/DDDT.S185418
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Article: Panax Notoginseng flower saponins (PNFS) inhibit LPS-stimulated NO overproduction and iNOS gene overexpression via the suppression of TLR4-mediated MAPK/NF-kappa B signaling pathways in RAW264.7 macrophages.

Peng, Xiao-Xu / Zhang, Shu-Hui / Wang, Xiao-Ling / Ye, Ting-Jie / Li, Hua / Yan, Xiao-Feng / Wei, Li / Wu, Zhong-Ping / Hu, Jing / Zou, Chun-Pu / Wang, You-Hua / Hu, Xu-Dong

Chinese medicine

2015 Volume 10, Page(s) 15

Abstract: Background: Panax Notoginseng flower saponins (PNFS) are the main active component of Panax notoginseng (Burk) F. H. Chen flower bud (PNF) and possess significant anti-inflammatory efficacy. This study aims to explore the mechanisms underlying PNFS' ... ...

Abstract	Background: Panax Notoginseng flower saponins (PNFS) are the main active component of Panax notoginseng (Burk) F. H. Chen flower bud (PNF) and possess significant anti-inflammatory efficacy. This study aims to explore the mechanisms underlying PNFS' antiflammatory action in RAW264.7 macrophages. Methods: A cell counting kit-8 assay was used to determine the viability of RAW264.7 macrophages. Anti-inflammation effects of PNFS in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages were measured based on the detection of nitric oxide (NO) overproduction (Griess method, DAF-FM DA fluorescence assay and NO2 (-) scavenging assay), and interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha gene overexpression (real-time PCR and ELISA). Inducible nitric oxide synthase (iNOS) gene overexpression was determined by real-time PCR and western blotting. iNOS enzyme activity was also assayed. The mechanisms underlying the suppression of iNOS gene overexpression by PNFS were explored using real-time PCR and western blotting to assess mRNA and protein levels of components of the Toll-like receptor 4 mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K)/Akt, and nuclear factor-kappa B (NF-kappa B) signaling pathways. Results: PNFS (50, 100, 200 μg/mL) significantly reduced LPS-induced overproduction of NO (P < 0.001, P < 0.001, P < 0.001) and IL-6 (P = 0.103, P < 0.001, P < 0.001), but did not affect TNF-alpha overproduction. PNFS (50, 100, 200 μg/mL) also markedly decreased LPS-activated iNOS (P < 0.001, P < 0.001, P < 0.001) and TLR4 gene overexpression (P = 0.858, P = 0.046, P = 0.005). Furthermore, treatment with PNFS (200 μg/mL) suppressed the phosphorylation of MAPKs including P38 (P = 0.001), c-Jun N-terminal kinase (JNK) (P = 0.036) and extracellular-signal regulated kinase (ERK) 1/2 (P = 0.021). PNFS (200 μg/mL) inhibited the activation of the NF-kappa B signaling pathway by preventing the phosphorylation of inhibitor of NF-kappa B alpha (I-kappa B alpha) (P = 0.004) and P65 (P = 0.023), but PNFS (200 μg/mL) could not activate the LPS-induced PI3K-Akt signaling pathway. Conclusions: PNFS significantly down-regulated iNOS gene overexpression and thereby decreased NO overproduction via the inhibition of TLR4-mediated MAPK/NF-kappa B signaling pathways, but not the PI3K/Akt signaling pathway.
Language	English
Publishing date	2015-07-01
Publishing country	England
Document type	Journal Article
ZDB-ID	2260322-0
ISSN	1749-8546
ISSN	1749-8546
DOI	10.1186/s13020-015-0045-x
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Article ; Online: Effect of Yiguanjian decoction on cell differentiation and proliferation in CCl₄-treated mice.

Wang, Xiao-Ling / Jia, Dong-Wei / Liu, Hui-Yang / Yan, Xiao-Feng / Ye, Ting-Jie / Hu, Xu-Dong / Li, Bo-Qin / Chen, Yong-Liang / Liu, Ping

World journal of gastroenterology

2012 Volume 18, Issue 25, Page(s) 3235–3249

Abstract: Aim: To investigate the cellular mechanisms of action of Yiguanjian (YGJ) decoction in treatment of chronic hepatic injury.: Methods: One group of mice was irradiated, and received enhanced green fluorescent protein (EGFP)-positive bone marrow ... ...

Abstract	Aim: To investigate the cellular mechanisms of action of Yiguanjian (YGJ) decoction in treatment of chronic hepatic injury. Methods: One group of mice was irradiated, and received enhanced green fluorescent protein (EGFP)-positive bone marrow transplants followed by 13 wk of CCl₄ injection and 6 wk of oral YGJ administration. A second group of Institute for Cancer Research mice was treated with 13 wk of CCl₄ injection and 6 wk of oral YGJ administration. Liver function, histological changes in the liver, and Hyp content were analyzed. The expression of α-smooth muscle actin (α-SMA), F4/80, albumin (Alb), EGFP, mitogen-activated protein kinase-2 (PKM2), Ki-67, α fetoprotein (AFP), monocyte chemotaxis protein-1 and CC chemokine receptor 2 were assayed. Results: As hepatic damage progressed, EGFP-positive marrow cells migrated into the liver and were mainly distributed along the fibrous septa. They showed a conspicuous coexpression of EGFP with α-SMA and F4/80 but no coexpression with Alb. Moreover, the expression of PKM2, AFP and Ki-67 was enhanced dynamically and steadily over the course of liver injury. YGJ abrogated the increases in the number of bone marrow-derived fibrogenic cells in the liver, inhibited expression of both progenitor and mature hepatocyte markers, and reduced fibrogenesis. Conclusion: YGJ decoction improves liver fibrosis by inhibiting the migration of bone marrow cells into the liver as well as inhibiting their differentiation and suppressing the proliferation of both progenitors and hepatocytes in the injured liver.
MeSH term(s)	Actins/metabolism ; Administration, Oral ; Albumins/metabolism ; Animals ; Antigens, Differentiation/metabolism ; Biomarkers/metabolism ; Bone Marrow Cells/drug effects ; Bone Marrow Cells/metabolism ; Bone Marrow Transplantation ; Carbon Tetrachloride ; Cell Differentiation/drug effects ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Chemical and Drug Induced Liver Injury/drug therapy ; Chemical and Drug Induced Liver Injury/etiology ; Chemical and Drug Induced Liver Injury/metabolism ; Chemical and Drug Induced Liver Injury/pathology ; Chemokine CCL2/metabolism ; Drugs, Chinese Herbal/administration & dosage ; Drugs, Chinese Herbal/pharmacology ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Ki-67 Antigen/metabolism ; Liver/drug effects ; Liver/metabolism ; Liver/pathology ; Liver Cirrhosis, Experimental/chemically induced ; Liver Cirrhosis, Experimental/drug therapy ; Liver Cirrhosis, Experimental/metabolism ; Liver Cirrhosis, Experimental/pathology ; Liver Regeneration/drug effects ; Male ; Mice ; Mice, Inbred ICR ; Mice, Transgenic ; Mitogen-Activated Protein Kinase 1/metabolism ; Receptors, CCR2/metabolism ; Time Factors ; alpha-Fetoproteins/metabolism
Chemical Substances	Actins ; Albumins ; Antigens, Differentiation ; Biomarkers ; Ccl2 protein, mouse ; Ccr2 protein, mouse ; Chemokine CCL2 ; Drugs, Chinese Herbal ; Ki-67 Antigen ; Receptors, CCR2 ; alpha-Fetoproteins ; alpha-smooth muscle actin, mouse ; enhanced green fluorescent protein ; monocyte-macrophage differentiation antigen ; yiguanjian decoction ; Green Fluorescent Proteins (147336-22-9) ; Carbon Tetrachloride (CL2T97X0V0) ; Mapk1 protein, mouse (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24)
Language	English
Publishing date	2012-07-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2185929-2
ISSN	2219-2840 ; 1007-9327
ISSN (online)	2219-2840
ISSN	1007-9327
DOI	10.3748/wjg.v18.i25.3235
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Article: Analyzing the potential therapeutic mechanism of Huashi Baidu Decoction on severe COVID-19 through integrating network pharmacological methods.

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Article ; Online: High mobility group box-1 release from H

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Article: The Study of Yin-Chen-Hao-Tang Preventing and Treating Alcoholic Fatty Liver Disease through PPAR Signaling Pathway Based on Network Pharmacology and RNA-Seq Transcriptomics.

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Article ; Online: Adipose-Specific Lipin-1 Overexpression Renders Hepatic Ferroptosis and Exacerbates Alcoholic Steatohepatitis in Mice.

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Article ; Online: Intestinal SIRT1 Deficiency Protects Mice from Ethanol-Induced Liver Injury by Mitigating Ferroptosis.

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Article ; Online: Total extract of Xin Jia Xuan Bai Cheng Qi decoction inhibits pulmonary fibrosis via the TGF-β/Smad signaling pathways in vivo and in vitro.

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Article: Panax Notoginseng flower saponins (PNFS) inhibit LPS-stimulated NO overproduction and iNOS gene overexpression via the suppression of TLR4-mediated MAPK/NF-kappa B signaling pathways in RAW264.7 macrophages.

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Article ; Online: Effect of Yiguanjian decoction on cell differentiation and proliferation in CCl₄-treated mice.

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