虎杖对肾缺血-再灌注损伤大鼠肾组织内皮素和核转录因子的影响

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目的:探讨虎杖对肾缺血-再灌注损伤大鼠肾脏的保护作用及其机制。方法:健康雄性SD大鼠72只,随机分为4组:假手术组、缺血再-灌注模型组、虎杖及虎杖苷预处理组。采用切除大鼠右侧肾脏,左侧肾蒂夹闭60min制作肾缺血-再灌注模型。在缺血前10 min、再灌注6、12 h后分别检测血清肌酐(Scr)、尿素氮(BUN)的含量,免疫组化法检测肾组织内皮素(ET)和核转录因子(NF-κB),观察肾组织的病理变化,并分别进行比较。结果:缺血-再灌注后,治疗组大鼠肾组织病理变化轻于模型组,模型组大鼠肾组织中ET、NF-κB明显表达,BUN和Cr含量明显上升;虎杖及虎杖苷处理组肾组织中NF-κB表达均受到抑制,虎杖预处理组肾组织中ET表达受到抑制,与模型组比较,虎杖及虎杖苷预处理组BUN和Cr含量降低。结论:在肾缺血-再灌注损伤的过程中,虎杖及其有效组分虎杖苷可能通过抑制肾组织中ET、NF-κB表达,改善肾功能,具有保护肾缺血-再灌注损伤大鼠肾脏的作用。 Objective: To investigate the protective effect of Polygonum cuspidatum on kidney in rats with renal ischemia-reperfusion injury and its mechanism. METHODS: A total of 72 healthy male SD rats were randomly divided into 4 groups: sham operation group, ischemia-reperfusion model group, Polygonum cuspidatum and polydatin pretreatment group. The right kidney was removed from the rat and the left renal pedicle was clipped for 60 minutes to make a renal ischemia-reperfusion model. Serum creatinine (Scr) and urea nitrogen (BUN) levels were measured 10 min before ischemia and 6 and 12 h after reperfusion. Renal endothelin (ET) and nuclear transcription factor (NF-κB) were detected by immunohistochemistry. ), Observe the pathological changes of kidney tissue and compare them separately. RESULTS: After ischemia-reperfusion, the pathological changes of renal tissue in the treatment group were lighter than those in the model group. The expression of ET and NF-kappaB in the kidney tissue of the model group was significantly increased, and the contents of BUN and Cr were significantly increased. Polygonum cuspidatum and Polydatin treated group The expression of NF-κB in renal tissue was inhibited, and the expression of ET in kidney tissue of the Polygonum cuspidatum pretreatment group was inhibited. Compared with the model group, the contents of BUN and Cr in the Polygonum cuspidatum and pretreatment groups decreased. Conclusion: During the course of renal ischemia-reperfusion injury, Polygonum cuspidatum and its effective fraction of polydatin may inhibit renal ischemia-reperfusion injury in rats by inhibiting the expression of ET and NF-κB in kidney tissue and improving renal function. The role of the kidneys.
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