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安徽苷C减轻糖尿病肾病大鼠的足细胞损伤。

Anhuienoside C Attenuates Podocyte Injury in Diabetic Nephropathy Rats.

作者信息

Wang Chengjian, Jiang Yingsong, Yu Keping, Liu Ke, Wang Hao

机构信息

Department of Endocrinology, Chongqing General Hospital, University of Chinese Academy of Sciences, Chongqing, China.

Department of Nephrology, Chongqing General Hospital, University of Chinese Academy of Sciences, Chongqing, China.

出版信息

Dose Response. 2020 Sep 22;18(3):1559325820939010. doi: 10.1177/1559325820939010. eCollection 2020 Jul-Sep.

Abstract

OBJECTIVE

The present study evaluated the nephroprotective effects of anhuienoside C (AC) against diabetic nephropathy (DN) in rats.

MATERIAL AND METHODS

Diabetic nephropathy was induced by administration of a high-fat diet (HFD) for 8 weeks and intraperitoneal administration of streptozotocin (STZ; 30 mg/kg) at the end of the fourth week of this protocol. Effects of AC on blood glucose levels, renal function markers, and mediators of inflammation in the serum of DN rats were assessed.

RESULTS

Anhuienoside C treatment reduced the blood glucose levels and attenuated the increased levels of renal injury markers in DN rats. Anhuienoside C also increased podocyte counts; alleviated the changes in podocin, desmin, and nephrin protein levels; and ameliorated the altered pathophysiology in the kidney tissues induced by DN. Compared with the DN group, the levels of inflammatory markers and mediators of oxidative stress were reduced in the serum and kidney tissues of the AC-treated groups. Moreover, treatment with AC ameliorates the altered expression of podocin, nephrin, and desmin proteins in the renal tissue of HFD/STZ-induced kidney-injured rats.

CONCLUSION

In conclusion, AC protected against podocyte injury by regulating nuclear factor kappa-light-chain-enhancer of activated B cells/protein kinase B pathway in a rat model of DN.

摘要

目的

本研究评估了安徽苷C(AC)对大鼠糖尿病肾病(DN)的肾保护作用。

材料与方法

通过给予高脂饮食(HFD)8周,并在该方案第四周结束时腹腔注射链脲佐菌素(STZ;30mg/kg)诱导糖尿病肾病。评估了AC对DN大鼠血清中血糖水平、肾功能标志物和炎症介质的影响。

结果

安徽苷C治疗降低了DN大鼠的血糖水平,并减轻了肾损伤标志物水平的升高。安徽苷C还增加了足细胞计数;减轻了足突蛋白、结蛋白和nephrin蛋白水平的变化;并改善了DN诱导的肾组织病理生理学改变。与DN组相比,AC治疗组血清和肾组织中炎症标志物和氧化应激介质水平降低。此外,AC治疗改善了HFD/STZ诱导的肾损伤大鼠肾组织中足突蛋白、nephrin和结蛋白的表达改变。

结论

总之,在DN大鼠模型中,AC通过调节活化B细胞的核因子κB轻链增强子/蛋白激酶B途径来保护足细胞免受损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e86d/7513418/51596b3cc1b4/10.1177_1559325820939010-fig1.jpg

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