当前位置：
X-MOL 学术
›
Food Funct.
›
论文详情
Our official English website, www.x-mol.net, welcomes your
feedback! (Note: you will need to create a separate account there.)
The renoprotective effect of diosgenin on aristolochic acid I-induced renal injury in rats: impact on apoptosis, mitochondrial dynamics and autophagy.
Food & Function ( IF 5.1 ) Pub Date : 2020-07-25 , DOI: 10.1039/d0fo00401d Chengni Jin 1 , Xin Miao 1 , Yujie Zhong 1 , Jiahui Han 1 , Qi Liu 1 , Jiachang Zhu 1 , Xiaodong Xia 1 , Xiaoli Peng 2
Food & Function ( IF 5.1 ) Pub Date : 2020-07-25 , DOI: 10.1039/d0fo00401d Chengni Jin 1 , Xin Miao 1 , Yujie Zhong 1 , Jiahui Han 1 , Qi Liu 1 , Jiachang Zhu 1 , Xiaodong Xia 1 , Xiaoli Peng 2
Affiliation
|
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.
中文翻译：
薯gen皂甙元对马兜铃酸I致大鼠肾损伤的肾脏保护作用：对细胞凋亡，线粒体动力学和自噬的影响。
马兜铃酸I（AA-I）仍然是马兜铃酸肾病（AAN）的主要原因，但是很少有预防和治疗策略。在这项工作中，研究了薯os皂甙元（一种在多种植物中大量分布的甾体皂苷）对AA-1诱导的肾损伤的肾脏保护作用及其潜在机制。在暴露于10 mg kg -1 d -1的两个小时之前，对Sprague-Dawley大鼠进行胃内注射30 mg kg -1 d -1薯gen皂甙元连续4周观察AA-1，并观察其组织学变化，肾和肝功能，细胞凋亡，自噬和相关途径。结果表明薯di皂苷元减轻了AA-I引起的肾脏组织学损伤，包括轻度水肿性肾小管排列紊乱和肾小管腔扩大。在所有治疗组中均未观察到肝组织结构的明显变化。此外，薯os皂苷元上调了Bcl-2的表达而下调了Bax，随后抑制了AIF表达和Caspase-3的裂解形式，从而减轻了由AA-1触发的细胞凋亡。薯os皂素还通过增加包括DRP1和MFN2在内的线粒体动力学相关蛋白的表达，减轻了AA-I引起的肾线粒体动力学障碍。薯os皂甙元抑制AA-I诱发的自噬通过ULK1介导的mTOR途径抑制作用。总体而言，这些结果表明薯di皂苷元具有抗AA-I引起的肾损伤的保护作用，并且可能是预防AA-I诱导的AAN的潜在药物。
更新日期：2020-09-23
中文翻译：
薯gen皂甙元对马兜铃酸I致大鼠肾损伤的肾脏保护作用：对细胞凋亡，线粒体动力学和自噬的影响。
马兜铃酸I（AA-I）仍然是马兜铃酸肾病（AAN）的主要原因，但是很少有预防和治疗策略。在这项工作中，研究了薯os皂甙元（一种在多种植物中大量分布的甾体皂苷）对AA-1诱导的肾损伤的肾脏保护作用及其潜在机制。在暴露于10 mg kg -1 d -1的两个小时之前，对Sprague-Dawley大鼠进行胃内注射30 mg kg -1 d -1薯gen皂甙元连续4周观察AA-1，并观察其组织学变化，肾和肝功能，细胞凋亡，自噬和相关途径。结果表明薯di皂苷元减轻了AA-I引起的肾脏组织学损伤，包括轻度水肿性肾小管排列紊乱和肾小管腔扩大。在所有治疗组中均未观察到肝组织结构的明显变化。此外，薯os皂苷元上调了Bcl-2的表达而下调了Bax，随后抑制了AIF表达和Caspase-3的裂解形式，从而减轻了由AA-1触发的细胞凋亡。薯os皂素还通过增加包括DRP1和MFN2在内的线粒体动力学相关蛋白的表达，减轻了AA-I引起的肾线粒体动力学障碍。薯os皂甙元抑制AA-I诱发的自噬通过ULK1介导的mTOR途径抑制作用。总体而言，这些结果表明薯di皂苷元具有抗AA-I引起的肾损伤的保护作用，并且可能是预防AA-I诱导的AAN的潜在药物。
京公网安备 11010802027423号