黄芪甲苷对被动型Heymann肾炎大鼠PERK通路的影响
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R692.3

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温州市科技计划项目(Y20160308)


Astragaloside IV Has Effect on PERK Pathway in Rats with Passive Heymann Nephritis
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    摘要:

    目的:观察黄芪甲苷对被动型Heymann肾炎大鼠PERK通路的影响。方法:用羊抗大鼠Fx1A抗体血清尾静脉注射制备被动型Heymann肾炎大鼠模型。40只SD大鼠随机分为正常对照组、模型组、黄芪甲苷低剂量组、黄芪甲苷高剂量组和贝那普利组。造模成功后各治疗组灌胃给药4周。定期检测24 h尿蛋白定量。4周后处死所有大鼠,采血检测血清白蛋白,PASM染色观察肾组织病理学改变,免疫组化检测肾组织磷酸化蛋白激酶R样内质网激酶(p-PERK)、磷酸化真核细胞翻译起始因子2α(p-eIF2α)的表达,Western blot检测肾组织中葡萄糖调节蛋白78(GRP78) 的表达。结果:模型组大鼠24 h尿蛋白定量较正常对照组显著升高(P<0.05),并随着时间推移蛋白尿逐渐增多,至4周后达到高峰。在给药4周后,与正常对照组比较,模型组大鼠肾组织p-PERK、p-eIF2α、GRP78表达明显升高,血清白蛋白明显降低,差异均有统计学意义(P<0.05)。与模型组比较,黄芪甲苷高剂量组及贝那普利组大鼠24 h尿蛋白显著减少,肾组织p-PERK、p-eIF2α、GRP78表达显著减少,血清白蛋白显著升高,差异均有统计学意义(P<0.05)。结论:黄芪甲苷可能通过抑制内质网应激(ERS)中的PERK通路缓解被动型Heymann肾炎大鼠肾脏损伤。

    Abstract:

    Objective:To observe the effect of astragaloside IV on PERK pathway in rats with passive Heymann nephritis.Methods:The rat model of passive Heymann nephritis was established by tail intravenous injection of anti-Fx1A serum.Forty SD rats were randomly divided into the normal control group,the model group,the low-dose astragaloside IV group,the high-dose astragaloside IV group and the benazepril group.After the success of model establishment,each treatment group received intragastric administration for 4 weeks.Detected 24-h urinary protein quantification periodically.After 4 weeks,sacrificed all the rats,collected blood to detect serum albumin,observed the renal pathological changes by PASM,detected the expression of phosphorylated protein kinase R-like ER kinase(p-PERK)and phosphorylated eukaryotic translation initiation factor 2α(p-eIF2α)in renal tissues by immunehistochemistry,and detected the expression of glucose-regulated protein 78(GRP78)in renal tissues by Western blot.Results:24-h urinary protein quantification of rats in the model group was significantly higher than that in the normal control group(P < 0.05),and the urine protein was gradually increased as time went by,which reached its peak after 4 weeks.After administration for 4 weeks,comparing with the normal control group,the expression of p-PERK,p-eIF2α and GRP78 in the renal tissues of rats in the model group was evidently higher,serum albumin was decreased evidently,differences being significant(P < 0.05).Comparing with the model group,24-h urinary protein quantification of rats in the high-dose astragaloside IV group and the benazepril group were significantly decreased,the expression of p-PERK,p-eIF2α and GRP78 in the renal tissues was significantly decreased,and serum albumin was significantly increased,differences being significant(P< 0.05).Conclusion:Astragaloside IV may relieve the renal damage resulting from passive Heymann nephritison by inhibiting PERK pathway in endoplasmic reticulum stress(ERS).

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项协隆,邵思思,陈宇,陈春,董飞侠.黄芪甲苷对被动型Heymann肾炎大鼠PERK通路的影响[J].新中医,2018,50(4):10-14

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  • 在线发布日期: 2018-04-10
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