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Possible role of mitochondrial injury in Caulis Aristolochia manshuriensis-induced chronic aristolochic acid nephropathy.

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机构: [1]Department of Nephrology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, Guangdong, China, [2]Key Laboratory of Nephrology, Ministry of Health and Guangdong Province, Guangzhou, Guangdong, China [3]Department of Nephrology, Shenzhen Traditional Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen, Guangdong, China
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关键词: Proximal tubular epithelial cells apoptosis regeneration disorder

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The proximal tubular epithelial cells (PTECs) are the primary target of aristolochic acids and especially vulnerable to mitochondrial injury from insults of toxic xenobiotics. This study aimed to investigate the possible role of mitochondrial injury in Caulis Aristolochia manshuriensis (CAM)-induced aristolochic acid nephropathy (AAN). Male Sprague-Dawley rats were gavaged with CAM extract every other week for 1, 4, 8 and 12 weeks, respectively. The rats in the model group showed chronic AAN as evidenced by worsening kidney function evaluated by blood urea nitrogen, creatinine and proteinuria levels, and severe tubulointerstitial injury marked by massive tubular atrophy and interstitial fibrosis in kidney tissues. Moreover, overt apoptosis and impaired regeneration of PTECs were observed in AAN rats. Furthermore, the study revealed that mitochondria in PTECs were fragmented into small, punctuate suborganelles in AAN rats. Two mitochondrial respiratory chain proteins, mitochondrial DNA (mtDNA)-encoded cytochrome c oxidase subunit І (COX-І) and nuclear DNA-encoded nicotinamide adenine dinucleotide dehydrogenase (ubiquinone)-1β subcomplex 8 (NDUFβ8), were both down-regulated after one week of CAM treatment. However, with AAN progression, NDUFβ8 level restored, while COX-І level maintained low. Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), master regulator of mitochondrial biogenesis, was significantly down-regulated at week 4 and week 8, but significantly up-regulated at week 12. In addition, mtDNA copy number reduced markedly along with AAN progression. A rat model of chronic AAN was successfully reproduced by gavage with CAM extract. Dynamic changes of mitochondrial injury induced by CAM might contribute to the AAN progression.

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出版当年[2016]版:
大类 | 4 区 医学
小类 | 4 区 化学综合 4 区 药学 4 区 毒理学
最新[2025]版:
大类 | 4 区 医学
小类 | 3 区 化学:综合 4 区 药学 4 区 毒理学
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出版当年[2015]版:
Q3 CHEMISTRY, MULTIDISCIPLINARY Q3 PHARMACOLOGY & PHARMACY Q4 TOXICOLOGY
最新[2023]版:
Q3 CHEMISTRY, MULTIDISCIPLINARY Q3 PHARMACOLOGY & PHARMACY Q3 TOXICOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2015版] 出版当年五年平均 出版前一年[2014版] 出版后一年[2016版]

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第一作者机构: [1]Department of Nephrology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, Guangdong, China, [2]Key Laboratory of Nephrology, Ministry of Health and Guangdong Province, Guangzhou, Guangdong, China [3]Department of Nephrology, Shenzhen Traditional Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen, Guangdong, China
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通讯机构: [1]Department of Nephrology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, Guangdong, China, [2]Key Laboratory of Nephrology, Ministry of Health and Guangdong Province, Guangzhou, Guangdong, China [*1]Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510080, China.
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