Hepatic fibrosis by disrupting angiotensin II signaling by means of down-regulation of angiotensin > 자유게시판

Hepatic fibrosis by disrupting angiotensin II signaling by using down-regulation of angiotensin II receptor kind 1, ERK, and c-Jun phosphorylation [98]. Andrographolide from a. paniculata lowered theDuval et al. Chinese Medication (2014) 9:Site four ofTable 1 Inhibitory mechanisms of hepatic stellate cell activation through medicinal plantsMedicinal vegetation C. longa [27-46] S. marianum [47-54] G. biloba [55-60] S. miltiorrhiza [46,forty nine,61-100] Bioactive compounds/extracts Curcumin Silymarin G. biloba extract, EGb761 Water extract of S. 4CzIPN miltiorrhiza; salvianolic acid A; salvianolic acid B; tert-Butyl (2-bromothiazol-5-yl)carbamate magnesium lithospermate B; tanshinone IIA; IH764-3 Glycyrrhizin; 18-glycyrrhizin; glycyrrhizic acid Baicalin Saikosaponin-A; saikosaponin-D Ethanol extract of P. rheedii Wight; ethanol extract of P. niruri Berberine Ginsenoside Rg1; ginsenoside Rb1; P. notoginseng saponins; 25-OCH3-PPD Andrographolide Caffeine; 1,7-dimethylxanthine; theophylline; theobromine Specific fibrogenic pathways TGF-1a; CTGFb; PDGFc; TGF-d; VEGFe; AGEf; leptin; LDLg; insulin; HIF-1h; PGFi TGF-1a; CTGFb TGF-1a; CTGFb; PAFj; endothelin-1 TGF-1a; CTGFb; PDGFc; MCP-1k; endothelin-1; angiotensin II TGF-1a TGF-1a TGF-1a TGF-1a TGF-1a TGF-1a; PDGFc TGF-1a TGF-1a; CTGFb; VEGFe; PDGFcG. glabra [101-104] S. baicalensis [105-107] B. falcatum [32,108,109] Phyllanthus species [110,111] B. aristata [112-114] P. notoginseng [105,115-118] A. paniculata [119] Coffea species [120-130]a Transforming progress issue beta one, bconnective tissue development variable, cplatelet derived PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/9282946 advancement factor, dtransforming progress component alpha, evascular endothelial progress component, fadvance glycation end-product, glow-density lipoprotein, hhypoxia-inducible factor-1, iplacental expansion issue, jplatelet activate aspect, kmonocyte chemotactic protein-1.hepatic degree of cannabinoid receptor one through inactivation of c-Jun N-terminal kinases as well as the ERK phosphorylation cascade [119]. HSC proliferation is mediated by unique proteins, such as PDGF, CTGF, VEGF, and TGF- as a result of many sign molecules, these as ERK and focal adhesion kinase (FAK) [12]. Some plant extracts goal these growth things and their respective signaling pathways to lower the proliferative response of HSCs. CTGF is inhibited by curcumin [34,36], silymarin [54], G. biloba extract [59], Salvia extract [49,76], and caffeine [120,128-130] by way of inhibition of TGF- signaling. Moreover, curcumin was revealed to lower the promoter exercise PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/12711626 of CTGF and suppress its gene expression by lessening NF-B exercise [36]. NF-B was inhibited by suppression of ERK exercise and suppression of Toll like receptor-4 gene expression by means of PPAR activation [36]. PDGF and its receptor PDGF-R had been uncovered to become down-regulated by curcumin [35,37], salvianolic acid A [63] and B [92], coffee [123], and ginsenoside Rg1 [116]. Ginsenoside Rg1 down-regulated the expression of PDGF-R by decreasing NF-B activity [116]. Unique bioactive compounds from S. miltiorrhiza lowered HSC proliferation. The monomer IH764-3 inhibited HSC proliferation by down-regulating FAK and ERK expression [64,sixty five,80], though salvianolic acid B attenuated PDGFinduced c-Jun N-terminal kinases, p38, and protein kinase C delta phosphorylations [95]. VEGF and its receptors were suppressed by curcumin [45] and coffee [122], which could also clarify theiramelioration of angiogenesis inside the fibrotic liver. Also, curcumin lowered TGF- concentrations [43]. Cyclins, and cyclin inhibitors, are necessary proteins to the regulate of the mobile cycle,.