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Protective Effects of Butyrate on Renal Ischemia-Reperfusion Injury in Rats

机译:丁酸盐对大鼠肾缺血再灌注损伤的保护作用

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Background: Renal ischemia-reperfusion injury (IRI) usually causes acute kidney injury. There is an urgent need to develop an effective agent to prevent renal IRI. This study aimed to examine the effect of butyrate on renal IRI in rats. Materials and Methods: Rats were randomly assigned into 3 groups (10 rats in each group): the sham group, the IRI group, and the butyrate group. Rats were injected intravenously with 300 mg/kg of sodium butyrate in the butyrate group and with a saline solution in the sham group and IRI group 30 min before renal ischemia. After 24 h of reperfusion, renal function and histologic damage were examined. Myeloperoxidase (MPO) activity assay, in situ apoptosis examination, enzyme-linked immunosorbent assay, immunohistochemical assay, and Western blot were performed as well. Results: Butyrate pretreatment significantly reduced renal dysfunction and histologic damage induced by renal IRI. Butyrate pretreatment caused a significant attenuation of neutrophil infiltration, which was reflected by the reduction of renal MPO activity. Butyrate also reduced apoptotic tubular cell death and improved caspase-3 activation. The expression of TNF-alpha was decreased following butyrate pre-treatment. Conclusions: Butyrate pretreatment protects rats from renal IRI by inhibiting inflammation and apoptosis. Therefore, butyrate may be a potential therapeutic agent for preventing renal IRI. (C) 2019 S. Karger AG, Basel
机译:背景:肾缺血再灌注损伤(IRI)通常会导致急性肾损伤。迫切需要开发有效的药剂以防止肾IRI。本研究旨在检测丁酸盐对大鼠肾IRI的影响。材料和方法:将大鼠随机分配到3组(每组10只大鼠):假组,IRI组和丁酸酯组。在丁酸盐基团中静脉内用300mg / kg丁酸钠静脉内注射大鼠,并在假手术组和IRI组中盐水溶液30分钟,肾脏缺血30分钟。在再灌注24小时后,检查肾功能和组织学损伤。肌释放酶(MPO)活性测定,原位凋亡检查,酶联免疫吸附测定,免疫组化测定和蛋白质印迹也是如此。结果:丁酸盐预处理显着降低了肾IRI诱导的肾功能紊乱和组织学损伤。丁酸盐预处理引起了中性粒细胞渗透的显着衰减,这被肾MPO活性的减少反映。丁酸盐还降低了凋亡管状细胞死亡和改善的Caspase-3活化。丁酸盐预处理后,TNF-α的表达减少。结论:通过抑制炎症和凋亡,丁酸盐预处理通过抑制炎症和细胞凋亡来保护来自肾IRI的大鼠。因此,丁酸盐可以是预防肾IRI的潜在治疗剂。 (c)2019年S. Karger AG,巴塞尔

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