Résumé
Objective: To investigate the impact and its possible mechanism of hydrogen sulfide (H2S) on myocardial collagen remodeling in experimental rats with diabetic mellitus (DM). Methods: Rat’s DM model was established by intraperitoneal injection of STZ at 40 mg/kg. A total of 40 SD rats were randomly divided into 4 groups:Control group, DM group, DM+NaHS group, in which NaHS worked as exogenous donor of H2S and NaHS control group. n=10 in each group, all animals were treated for 8 weeks. The cardiac collagen deposition was observed by Masson staining, protein expressions of cardiac collagen types I, III, IV and transforming growth factorβ1 (TGF-β1), connective tissue growth factor (CTGF) were examined by Western blot analysis. Results: Compared with Control group, DM group showed increased protein expressions of cardiac collagen types I and III, up-regulated expressions of TGF-β1 and CTGF, P Conclusion: H2S may improve the myocardial collagen remodeling in experimental DM rats, the mechanism might be related to the down-regulation of TGF-β1 and CTGF expression.
Résumé
Objectives To observe the expressions ofα-smooth muscle actin (a-SMA) and type III collagen (Col-III) of tubuloin-terstitial ifbrosis(TIF) induced by unilateral ureteral obstruction (UUO) in rat and the intervention effect of supplemental hydrogen sul-ifde (H2S). Methods Ninety-six male Sprague-Dawley rats were randomly divided into 4 groups, sham-operated group, UUO model group, NaHS low-dose group and high-dose group. TIF rat model was established via UUO. After UUO operation, low-dose and high-dose group were intraperitoneally injected twice a day with 1.4μmol/kg and 7.0μmol/kg NaHS, respectively. Sham-operated group and UUO model group were given an equivalent volume of normal saline. Eight rats in each group were killed randomly at 7, 14 and 21 days after UUO operation. The concentration of plasma H2S was detected using deproteinization. Renal tubulointerstitial damage was evaluated with routine Hematoxylin and Eosin staining and Masson staining under microscope. The expressions ofα-SMA, Col-III were measured with immunohistochemistry. Results Compared with sham-operated group, renal tubulointerstitial injury was severer in UUO model group and was alleviated after intervention of NaHS. There was signiifcant difference in tubulointerstitial injury among all groups (P0.05). Conclusions TIF induced by UUO is associated with decreased level of endogenous H2S. H2S supplementation can ameliorate the development of UUO-associated TIF in part through down-regulating the expressions ofα-SMA and Col-III in renal tissues. However, a dose dependent manner between the two doses of exogenous H2S supplementation was not observed.
Résumé
Objective: To investigate the effect of hydrogen sulifde (H2S) on the expression of CSE, NF-κB, and IL-8 mRNA in GES-1 cells withHelicobacter pylori (H. pylori) infection and to explore its mechanism on gastric mucosa inlfammation caused byH. pylori. Methods: GES-1 cells were cultured for 24 h and divided into a control group (neitherH. pylori nor NaHS), anH. pylori group, a NaHS group (which was further divided into 4 groups at 50, 100, 200, or 400 μmol/L NaHS), andH. pylori + NaHS group (which was further divided into 4 groups at 50, 100, 200, or 400 μmol/L NaHS). Each group was then cultured for 3, 6, or 12 h. The expression of CSE, NF-κB, and IL-8 mRNA was measured by RT-PCR, and their correlation was analyzed. Results: The expression of CSE, NF-κB, and IL-8 mRNA in GES-1 cells in theH. pylori group was higher than that in the control group. The expression of CSE in the 200 μmol/L NaHS group and 400 μmol/L NaHS group was lower than that of the control group (P0.05). The expression of CSE, NF-κB, and IL-8 mRNA in all groups of NaHS,H. pylori + 200 μmol/L NaHS group, andH. pylori + 400 μmol/L NaHS group was lower than that in theH. pylori group (P Conclusion:H. pylori can induce NF-κB and IL-8 mRNA expression and upregulate CSE mRNA expression. At 200 and 400 μmol/L, NaHS can suppressH. pylori-induced NF-κB and IL-8 mRNA expression and ameliorate the morphology ofH. pylori-induced GES-1 injury, which may protect gastric epithelial cells byH. pylori infection.