淫羊藿苷对自发性高血压大鼠肾损伤的改善作用及机制研究
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篇名: | 淫羊藿苷对自发性高血压大鼠肾损伤的改善作用及机制研究 |
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摘要: | 目的:观察淫羊藿苷(ICA)对自发性高血压大鼠(SHR)肾组织病理损伤的影响,并基于核因子κB(NF-κB)信号通路研究其作用机制。方法:将21只SHR随机均分为模型组和ICA低、高剂量组(20、40 mg/kg,记为 ICA-L、ICA-H组),另取7只同源京都大鼠(WKY)为对照组。各组大鼠ig给药,每日2次,连用11周;对照组和模型组大鼠ig等体积双蒸水。观察各组大鼠肾组织病理学变化;蛋白质印迹法检测肾组织磷酸化NF-κB-p65(p-NF-κB-p65)、NF-κB抑制蛋白(IκB)、肿瘤坏死因子α (TNF-α)蛋白的表达。结果:与对照组比较,模型组大鼠肾结构出现紊乱,肾小球囊腔狭窄且不规则;IκB蛋白的表达明显下调,p-NF-κB-p65、TNF-α蛋白的表达均明显上调(P<0.01)。与模型组比较,ICA-L、ICA-H组大鼠肾组织上述病理变化有所改善;ICA-L、ICA-H组IκB蛋白的表达均明显上调(P<0.05或P<0.01),ICA-H组大鼠p-NF-κB-p65、TNF-α蛋白的表达均明显下调(P<0.01),ICA-L组大鼠p-NF-κB-p65蛋白表达明显下调(P<0.05),而ICA-L组大鼠TNF-α蛋白表达差异无统计学意义(P>0.05)。结论: ICA具有改善SHR肾病理性损伤的作用,其机制可能与抑制NF-κB信号通路相关。 |
ABSTRACT: | OBJECTIVE: To observe the effect of pathological lesion of renal tissue in rats with spontaneous hypertension (SHR), and study its mechanisms based on nuclear factor κB (NF-κB) signaling pathway. METHODS: 21 SHR were randomly divided into model group and ICA low-dose, high-dose groups (20, 40 mg/kg, denoted by ICA-L, ICA-H groups); other 7 homologous Kyoto rats (WKY) were regarded as control group. All rats were intragastrically administrated, twice a day, for 11 weeks, rats in control group and model group received equal volume of double distilled water, ig. Pathological changes in renal tissue in each group were observed; Western blot method was used to detect protein expressions of p-NF-κB-p65, IκB and TNF-α in renal tissue. RESULTS: Compared with control group, model group showed disorder renal structure, narrow and irregular glomerular cysts; the protein expression of IκB was significantly down-regulated, protein expressions of p-NF-κB-p65 and TNF-α were significantly up-regulated (P<0.01). Compared with model group, the above-mentioned changes of rats showed improvement in ICA-L, ICA-H groups; the protein expression of IκB was significantly up-regulated in ICA-L, ICA-H groups (P<0.05 or P<0.01); the protein expressions of p-NF-κB-p65 and TNF-α were significantly down-regulated (P<0.01) in ICA-H groups; p-NF-κB-p65 protein expression was significantly down-regulated in ICA-L group (P<0.05); while there was no significant difference in TNF-α protein expression in ICA-L group (P>0.05). CONCLUSIONS: ICA plays a role in improving renal pathological lesion in SHR, and the mechanism may be related to inhibiting NF-κB signaling pathway. |
期刊: | 2017年第28卷第10期 |
作者: | 朱玲,钱志强,李叶丽,王俊逸,杨华,杨丹莉 |
AUTHORS: | ZHU Ling,QIAN Zhiqiang,LI Yeli,WANG Junyi,YANG Hua,YANG Danli |
关键字: | 淫羊藿苷;自发性高血压大鼠;肾组织;磷酸化核因子κB-p65;肿瘤坏死因子α |
KEYWORDS: | Icariin; Spontaneously hypertension rats; Renal tissue; p-NF-κB-p65; TNF-α |
阅读数: | 363 次 |
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