STF-083010对肾脏缺血-再灌注损伤的保护作用

目的 观察STF083010对急性肾缺血-再灌注损伤的作用,探讨其损伤保护作用的机制.方法 选择健康雄性SD大鼠30只,随机分为假手术组(打开腹腔)、I-R组(建立大鼠肾I-R损伤模型)与STF083010组.分别在缺血-再灌注24h后处死大鼠,取血液和肾组织.全自动生化仪检测各组血清尿素氮(BUN)及肌酐(Scr)水平.PAS染色观察大鼠肾组织病理变化,免疫组化检测肾脏组织中XBP1、GRP78蛋白的表达.Quantitative real-time PCR(QPCR)测定大鼠肾组织标本中XBP1、GRP78 mRNA水平.结果 I-R组肌酐、尿素氮水平与假手术组相比差异均有统计学意义(P＜0.05).STF-083010组与I-R组相比,差异亦有统计学意义(P＜0.05).PAS病理图片可见STF-083010组肾小管损伤较I-R组明显减轻(P＜0.05);免疫组化检测显示STF-083010组XBP1的表达较I-R组明显降低(P＜0.05),STF-083010组GRP78蛋白的表达较I/R组明显升高;QPCR结果显示STF-083010组XBP1 mRNA水平较I-R组明显降低(P＜0.05),STF-083010组GRP78 mRNA较I-R组明显升高(P＜0.05).结论 STF-083010可以对大鼠肾脏缺血-再灌注损伤性保护作用.

Protective effect of STF083010 on renal ischemia and reperfusion injury

Objective To investigate the effect and mechanism of STF083010 on renal ischemia and reperfusion injury.Methods Thirty male SD rats were divided into 3 groups:sham operated,I-R and STF080310.The blood and kidneys were harvested 24 h after reperfusion.Renal function and histologic changes of serum creatinine(SCr) and blood urea nitrogen(BUN) were assessed.PAS staining was observe rat kidney pathological changes.Immunohistochemical detection of XBP1 and GRP78 was measured in kidney tissue.XBP1 mRNA and GRP78 mRNA was measured by quantitative real-time PCR.Results The level of Scr and BUN in I-R group showed significant difference after 24 h reperfusion compared with sham group (P ＜ 0.05).The level of Scr and BUN in STF-083010 group had significant difference after 24 h reperfusion compared with I-R group (P ＜ 0.05).PAS straining revealed that STF-083010 significantly attenuated renal dysfunction and histologic damage caused by I-R injury(P ＜ 0.05).Immunohistochemical detection showed that STF-083010 group had decreased the level of XBP1 protein compared with I-R group obviously(P ＜0.05).QPCR revealed that STF-083010 group had decreased the level of XBP1 mRNA compared with I-R group(P ＜ 0.05).STF-083010 group had increased level of GRP78 mRNA compared with I-R group.Conclusion STF-083010 inhibitors can protect kidney function by increasing the release of inflammatory factors.