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[Effects of hydrogen sulfide on NO content and iNOS activity in diaphragm from type 1 diabetic rats]
Rui Yang1, Qiang Jia1, Shan-Feng Ma1
1Department of Physiology, Bengbu Medical College, Bengbu 233030, China.
Objective:
To investigate the effects of hydrogen sulfide (H2S) on nitric oxide (NO) content and inducible nitric oxide syn-thase (iNOS) activity in diaphragm from type 1 diabetic rats.
Methods:
Thirty-two male SD rats were randomly divided into four groups:nor-mal control group (NC), diabetes mellitus group (DM), DM treatment group (DM + NaHS) and NaHS control group (NaHS) (n=8). Rats were treated with streptozotocin 55 mg/kg by intraperitoneal injection to establish type 1 diabetic rat model. The fourth week after the model-ing, the rats in the DM + NaHS and NaHS groups were treated with 14μmol/kg NaHS solution by intraperitoneally injected. After treatment for 5 weeks, fasting blood glucose (FBG) and diaphragm weight (DW)/body weight (BW) were measured. The pathological changes of draphrag-matic tissues were observed by HE staining. The activity of iNOS was analyzed by spectrophotometric method, while the content of NO was measured by nitric acid reductase method. The iNOS expressions at mRNA and protein levels in diaphragmatic tissues were detected by RT-PCR and Western blot respectively.
Results:
Compared with the NC group, there was no significant difference in the various indexes in the NaHS group. While FBG was increased significantly, DW/BW was decreased obviously in the DM group. HE staining revealed obvious changes in diaphragmatic tissues. The activity of iNOS and the content of NO were increased. The levels of iNOS mRNA and protein were in-creased significantly. Compared with the DM group, DW/BW and pathological damages were improved in the DM + NaHS group. The activity of iNOS and NO content were decreased significantly. The levels of iNOS mRNA and protein were decreased obviously.
Conclusions:
Exoge-nous H2S can suppress iNOS activity and expression to decrease the content of NO, which improving the capacity of diaphragm in type 1 diabet-ic rats.
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