Hydrogen sulfide treatment protects against renal ischemia-reperfusion injury via induction of heat shock proteins in rats
محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 22، شماره: 1
سال انتشار: 1397
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 272
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شناسه ملی سند علمی:
JR_IJBMS-22-1_015
تاریخ نمایه سازی: 20 مهر 1398
چکیده مقاله:
Objective(s): Hydrogen sulfide (H2S) attenuates ischemia-reperfusion injury (IRI) in different organs. However, its mechanism of action in renal IRI remains unclear. The present study investigated the hypothesis that H2S attenuates renal IRI via the induction of heat shock proteins (HSPs).Materials and Methods: Adult Wistar rats were subjected to unilateral renal ischemia for 45 min followed by reperfusion for 6 hr. One group of rats underwent I/R without treatment, one group was administered 150 μmol/l sodium hydrosulfide (NaHS) prior to I/R, one group was injected with 100 mg/kg quercetin (an HSP inhibitor) intraperitoneally prior to I/R, and another group received quercetin prior to I/R and treatment with NaHS following I/R. Two other groups underwent a sham operation and one of them received 150 μmol/l NaHS following the sham operation whereas the other received no treatment. Renal function and histological changes were compared and relevant indices of oxidative stress, apoptosis, and inflammation were examined. Results: IRI increased serum creatinine and blood urea nitrogen concentrations, promoted lipid peroxidation by elevating malondialdehyde levels, suppressed superoxide dismutase activity, stimulated inflammation by inducing NF-kB, IL-2, and TLR-4 expression, and increased renal apoptosis. Levels of HSP70, heme-oxygenase-1 (HO-1) and HSP 27 were increased following IRI and reversed following H2S treatment. H2S attenuated changes observed in pathology, lipid peroxidation, inflammation, and apoptosis following IRI. The administration of quercetin reversed all protective effects of H2S. Conclusion: The present study indicated that H2S protected renal tissue against IRI induced lipid peroxidation, inflammation, and apoptosis, which may be attributed to the upregulation of HSP 70, HO-1, and HSP 27.
کلیدواژه ها:
Hydrogen sulfide ، Heat shock protein 70 ، Heat shock protein 27 ، Heme oxygenase 1 ، Ischemia-reperfusion injury ، Rat ، Renal
نویسندگان
Yang Du
Department of Urology, Renmin Hospital of Wuhan University, Hubei, China
Xiu-heng Liu
Department of Urology, Renmin Hospital of Wuhan University, Hubei, China
Heng-cheng Zhu
Physician, Department of Urology, Renmin Hospital of Wuhan University, Hubei, China
lei wang
Physician, Department of Urology, Renmin Hospital of Wuhan University, Hubei, China
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