食品科学 ›› 2019, Vol. 40 ›› Issue (9): 107-114.doi: 10.7506/spkx1002-6630-20171121-268

• 营养卫生 • 上一篇    下一篇

芹菜素对3-氯-1,2-丙二醇诱导的大鼠肾损伤及线粒体分裂融合的影响

钟玉杰,师振强,晋程妮,王晓瑞,李 璇,韩佳慧,薛 维,伍 鹏,彭晓丽*,夏效东*   

  1. 西北农林科技大学食品科学与工程学院,陕西 杨凌 712100
  • 出版日期:2019-05-15 发布日期:2019-05-28
  • 基金资助:
    国家自然科学基金面上项目(31571928)

Effect of Apigenin on 3-Chloro-1,2-propanediol Induced Renal Injury and Mitochondrial Fission and Fusion in Rats

ZHONG Yujie, SHI Zhenqiang, JIN Chengni, WANG Xiaorui, LI Xuan, HAN Jiahui, XUE Wei, WU Peng, PENG Xiaoli*, XIA Xiaodong*   

  1. College of Food Science and Engineering, Northwest A & F University, Yangling 712100, China
  • Online:2019-05-15 Published:2019-05-28

摘要: 通过研究功能因子芹菜素对食品加工污染物3-氯-1,2-丙二醇(3-chloro 1,2-propanediol,3-MCPD)诱导的大鼠线粒体分裂融合的影响,探讨芹菜素对3-MCPD诱导的大鼠肾损伤的保护机制。将36 只雄性SD大鼠随机分成对照组、溶剂(羧甲基纤维素钠)组、3-MCPD组和低、中、高剂量芹菜素组,给实验鼠单独灌胃3-MCPD(30 mg/kg mb)或3-MCPD联合不同剂量的芹菜素28 d。每天记录大鼠体质量、摄食量,灌胃处理28 d后,麻醉处死,解剖取肾、肝、脑。苏木精-伊红染色后,于显微镜下观察肾脏病理形态的变化,检测肾组织线粒体分裂融合及线粒体转录因子的表达水平。结果表明,芹菜素能缓解3-MCPD诱导的食欲不振、肾组织肿胀、肾脏质量指数的增加以及肾小管、集合管上皮细胞排列不齐,肾小球、肾小囊病变等现象。此外,芹菜素缓解了3-MCPD诱导的线粒体分裂基因FIS1、DRP1的上调表达和线粒体融合基因MFN1、MFN2表达的下调。芹菜素协同处理缓解了3-MCPD导致的线粒体转录因子PGC1、NRF1、TFAM基因表达水平的下降。蛋白表达水平测定结果也证实,芹菜素缓解了3-MCPD诱导的线粒体分裂水平的升高、融合水平的降低以及转录因子NRF2表达的下调。研究结果表明芹菜素通过上调3-MCPD诱导的线粒体转录因子表达水平,调节分裂融合状态,有效缓解3-MCPD导致的肾器官损伤。

关键词: 芹菜素, 3-氯-1, 2-丙二醇, 肾损伤, 线粒体分裂融合, 线粒体转录因子

Abstract: To assess the effect of apigenin (API), a functional food factor, on 3-chloro-1,2-propanediol (3-chloro 1, 2-propanediol, 3-MCPD)-induced mitochondrial fission and fusion, the protective effect of API on renal injury was investigated. A total of 36 male adult Sprague-Dawley rats were randomly divided into six groups of 6 animals each: control group, solvent control (sodium carboxymethyl cellulose) group, 3-MCPD group, and low-, middle- and high-dose apigenin group. Rats in the experimental groups were administrated via oral gavage with 3-MCPD (30 mg/kg mb) alone or in combination with apigenin at different doses for 28 days. Body mass and food intake were recorded daily during the experimental period. Finally, the rats were sacrificed to harvest kidney, liver and brain tissues. Rinal tissue sections, stained with hematoxylin and eosin, were observed by microscopy. Renal mitochondrial fission and fusion and transcription factor expression were examined. The results showed that apigenin significantly alleviated the loss of appetite, renal tissue swelling, the increase of kidney/body mass ratio, the irregularity of renal tubular and collecting ducts epithelium and glomerular and renal capsular lesions in rats exposed to 3-MCPD. In addition, apigenin significantly attenuated the up-regulation of DRP1 and FIS1 and the down-regulation of MFN1, MFN2, PGC1, NRF1 and TFAM. At the protein level, apigenin alleviated the increase of mitochondrial fission, the decrease of mitochondrial fusion and the down-regulation of transcription factor NRF2 induced by 3-MCPD. This study suggested that apigenin could protect rats from 3-MCPD induced renal injury via up-regulating the expression of mitochondrial transcription factors and alleviating abnormal mitochondrial fusion and fission.

Key words: apigenin, 3-chloro-1,2-propanediol, renal injury, mitochondrial fission and fusion, mitochondrial transcription factor

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