These proteins had no obvious difference between group S and group HF. In group LS, PI3K and p-Akt expressed more than group LY, but less than group S. Conclusion: These results suggest that PI3K/Akt signal pathway was closely related to the development of hepatic fibrosis and its inhibitor LY294002 could significantly improve hepatic fibrosis. In addition, we outline that
hydrogen sulfide could delay the progress of hepatic fibrosis and had protective effects on hepatic fibrosis by inhibiting morphology damage and decreasing type I and III collagen expression, and these protective effects might be related to PI3K/Akt signal pathway. Key Word(s): 1. hepatic fibrosis; 2. hydrogen selleck products sulfide; 3. PI3K/Akt pathway; Presenting Author: YONG ZHENG Additional Authors: QIANG REN, GANGWEI CHEN, RUI LI, XIA XU, HONGLI XU Corresponding Author: YONG ZHENG Affiliations: Department of Gastroenterology, First Affiliated Hospital of the Medical College, Shihezi University, Shihezi, Xinjiang; Department of Gastroenterology, The Medical College of Shihezi University, Shihezi, Xinjiang Objective: Hepatic fibrosis is the common pathological basis for the development of chronic liver disease, is the inevitable stage of formation of liver cirrhosis, then it is also the effective response when body was injured by exogenous and inflammatory factor caused liver injury. Hepatic stellate cells (HSC) was Selleckchem LEE011 advitated and proliferation then produce extra
cellular matrix (ECM) is the main characteristics of the disease. Our previous studies have shown that in the occurrence and development of liver fibrosis, with the disease progresses, the content of endogenous
H2S are gradually reduced, it can significantly delay the onset of liver fibrosis after exogenous give H2S donor. In this experiment, we discuss the influence of cell proliferation, apoptosis that PI3K/Akt signaling pathway to hydrogen sulfide (H2S) post-processing in vitro cultured rat hepatic stellate cells (HSC T6) and the effect of the expression of collagen type I, III, in turn to discuss hydrogen sulfide by the PI3K/Akt signal pathway in the mechanism of action of liver fibrosis. Methods: cultured HSC T6 in vitro, NaHS (donor Amino acid of H2S) post-processing and dispossessed by the PI3K/Akt pathway specific blocker that LY294002. Drugs′ intervention after 48 hours, then determined by MTT assay to detect HSC T6 cell proliferation; Using flow cytometry by Annexin V-FITC/PI amphophil cells to detect the HSC apoptosis rate and coloration by Hoechest 33342 to test HSC cell apoptosis; PCR method for quantitative detection of the expression of collagen type I, III mRNA in HSC. Results: Compared with normal control group, H2S promote cell proliferation is obviously in S group, NaHS in low concentration 50 μmol●L-1 group is the most significant difference (P < 0.05), but the effect on cell apoptosis was not significant (P > 0.05), the expression of collagen type I and III mRNA were reduced.