山药多糖对肾缺血再灌注损伤大鼠肾组织缺氧诱导因子-1α和血管内皮生长因子表达的影响

目的观察山药多糖对肾缺血再灌注损伤大鼠肾组织缺氧诱导因子-1α(HIF-1α)和血管内皮生长因子(VEGF)表达的影响,并探讨其作用机制。方法 SD大鼠随机分为假手术组、模型组、山药多糖组,制备肾缺血再灌注损伤大鼠模型,术前7 d,山药多糖组每日给予山药多糖(200 mg/kg)灌胃,假手术组和模型组每日给予等体积生理盐水灌胃,缺血再灌注6 h后,检测各组大鼠血尿素氮(BUN)和血肌酐(SCr)的含量,Western Blot法检测各组肾组织HIF-1α蛋白表达水平,RT-PCR法检测各组肾组织HIF-1α、VEGF mRNA表达水平。结果与假手术组比较,模型组和山药多糖组血清BUN、SCr含量升高(P0.01),肾组织HIF-1αmRNA、蛋白表达及VEGF mRNA表达升高(P0.01);与模型组比较,山药多糖组血清BUN、SCr含量降低(P0.01),肾组织HIF-1α蛋白、mRNA表达及VEGF mRNA表达升高(P0.01)。结论山药多糖对肾缺血再灌注损伤大鼠具有明显保护作用,其机制可能是通过上调肾组织HIF-1α表达进而诱导VEGF的表达而达到治疗作用。

Effect of Chinese Yam Polysaccharide on Expression of HIF-la and VEGF in Rats with Renal Ischemia Reperfusion Injury

Objective To observe the effect of Chinese yam polysaccharide on the expression of hypoxia inducible factor-1a （HIF-1a） and vascular endothelial growth factor （VEGF） in rats with renal ischemia reperfusion injury. Methods SD rats were randomly divided into sham operation group, model group and Chinese yam polysaccharide group. Renal ischemia reperfusion injury model in rats was prepared. Seven days before operation, Chinese yam polysaccharide group was gastrically administrated with yam polysaccharide （200 mg/kg） daily, sham operation group and model group with same volume of saline respectively. BUN and SCr were detected postoperative 6 h, the protein expression of HIF-1a in renal tissue was detected by Western Blot, and HIF-1a and VEGF mRNA expression in renal tissue were detected by RT-PCR. Results Compared with sham operation group, serum levels of BUN and SCr of model group and Chinese yam polysaccharides group increased （P 〈0.01）, and the mRNA and protein expression of HIF-l a, mRNA expression of VEGF in renal tissue increased （P〈0.01）. Compared with model group, serum levels of BUN and SCr of Chinese yam polysaccharide group decreased （P〈0.01）, and HIF-1a mRNA and protein expression, VEGF mRNA expression in renal tissue increased （P〈0.01）. Conclusion Chinese yam polysaccharide has obvious protective effect on renal ischemia reperfusion injury, which may be related with up-regulation of HIF-1a expression and induction of VEGF expression.