The renoprotective effect of diosgenin on aristolochic acid I-induced renal injury in rats: Impact on apoptosis, mitochondrial dynamics and autophagy

被引：0
|
作者：
Jin, Chengni [1 ]
Miao, Xin [1 ]
Zhong, Yujie [1 ]
Han, Jiahui [1 ]
Liu, Qi [1 ]
Zhu, Jiachang [1 ]
Xia, Xiaodong [1 ]
Peng, Xiaoli [1 ,2 ]
机构：
[1] College of Food Science and Engineering, Northwest AandF University, Yangling Shaanxi,712100, China
[2] Beijing Advanced Innovation Center for Food Nutrition and Human Health, Beijing Technology and Business University (BTBU), Beijing,100048, China
来源：
Food and Function | 2020年 / 11卷 / 09期
关键词：
Aristolochic acid I (AA-I) remains a leading cause of aristolochic acid nephropathy (AAN); however few prevention and treatment strategies exist. In this work; the nephroprotective effect of diosgenin; a steroidal saponin distributed abundantly in several plants; on AA-I-induced renal injury and its underlying mechanism were investigated. Sprague-Dawley rats were intragastrically administered with 30 mg kg-1 d-1 diosgenin two hours before exposure to 10 mg kg-1 d-1 AA-I for consecutive four weeks; and the histological change; the renal and liver function; apoptosis; autophagy and the involved pathways were investigated. The results showed that diosgenin relieved AA-I-induced renal histological damage; including mild edematous disorder of renal tubular arrangement and widening of renal tubular lumen. No obvious changes in the hepatic tissue structure were observed in all treatment groups. Moreover; diosgenin up-regulated the expression of Bcl-2 and down-regulated Bax; and subsequently inhibited AIF expression and the cleaved form of Caspase-3; thereby alleviating apoptosis triggered by AA-I. Diosgenin also mitigated AA-I-induced renal mitochondrial dynamics disorder by increasing the expression of mitochondrial dynamics-related proteins including DRP1 and MFN2. Diosgenin inhibited AA-I-evoked autophagy via ULK1-mediated inhibition of the mTOR pathway. Overall; these results suggest that diosgenin has a protective effect against AA-I-induced renal damage and it may be a potential agent for preventing AA-I-induced AAN. © 2020 The Royal Society of Chemistry;
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页码：7456 / 7467
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