https://www.selleckchem.com/pd-1-pd-l1.html cancer tissues indicates poor prognosis of patients, and the silencing of TrxR1 can inhibit the proliferation of gastric cancer cells. To investigate the effects of exogenous hydrogen sulfide (H S) on the hepatic fibrosis in diabetic mice and its mechanism. Twenty-four C57 male mice (weight 22±2 g) were randomly divided into three groups ( =8) ① Normal control group (Control) Mice were intraperitoneally injected equal amount of normal saline, the injection time was the same as that of the experimental groups; ② Diabetes model groups (HG) Streptozotocin (STZ) was injected intraperitoneally once according to body weight (150 mg/kg) to establish diabetes model; ③ NaHS treatment groups (HG + NaHS) Mice were intraperitoneally injected with NaHS (100 μmol/L·kg·d) once a day for 12 consecutive weeks. The hepatocyte injury was detected by HE staining; the hepatic fibrosis was observed through Masson staining; the protein expressions of cystathionine - β - synthetase (CBS), collagen-I (CoL-I), collagen-III (CoL-III) and matrix metalloproteinase-9 (MMP-9) were detected by Western blot. Compared with the control group, the damage and fibrosis of hepatocyte were significantly aggravated, the expression of CBS proteins was decreased ( ＜0.01), and the expression levels of CoL-I, CoL-III and MMP-9 proteins were increased ( ＜0.01) in the diabetic model group. Compared with the diabetic model group, the damage and fibrosis of hepatocyte were significantly lightened, the expression of CBS proteins was obviously increased ( ＜0.01), and the expression levels of CoL-I, CoL-III and MMP-9 proteins were markedly decreased ( ＜ 0.01). H S inhibits the hepatic fibrosis in diabetic mice, and its mechanism is related to the decrease of collagen and matrix metalloproteinase-9. H2S inhibits the hepatic fibrosis in diabetic mice, and its mechanism is related to the decrease of collagen and matrix metalloproteinase-9. To investigate the improved effects o