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《Journal of Medical Research》 2020-05
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Protective Effect of Apelin on Renal Tubular Mitochondria in Acute Kidney Injury

Wang Liyan;Guan Yiming;Diao Zongli;Department of Nephrology, Beijing Friendship Hospital, Capital Medical University;  
Objective To investigate the inhibitory effect of bioactive peptide apelin on tubular epithelial mitochondria in cisplatin-induced acute kidney injury(AKI). Methods Human proximal renal tubular epithelial cells were cultured in vitro and incubated with cisplatin(5μmol/L) and/or apelin-13(1μmol/L). Three experimental groups were set up: Control group, Cisplatin group, and Cisplatin +Apelin group. The mRNA expression of Sirt3 was detected by RT-PCR. The level of acetylation protein in mitochondria and expression of mitochondrial fission protein Drp1 and fusion protein OPA1 was detected by Western blot. AKI was induced by intraperitoneal injection of cisplatin(20 mg/kg) for one time in 8-week-old male wild-type mice. Apelin-13(0.1μmol/kg) or saline were injected intraperitoneally every day from the next day of cisplatin injection. Three experimental groups were set up: Control group, Cisplatin +Saline group and Cisplatin +Apelin group. The proximal tubular mitochondria was observed by transmission electron microscopy. Plasma creatinine(Cr) and urea nitrogen, as well as, kidney injure molecule(Kim-1) and neutrophil gelatinase-associated lipocalin(NGAL) in urine, were detected by ELISA kit. Results Cell experiments showed that the expression of Sirt3 mRNA was significantly lower and the level of acetylation protein in mitochondria was higher in Cisplatin group than that in Control group(all P0.05). The expression of mitochondrial fission protein Drp1 increased, meanwhile the expression of mitochondrial fusion protein OPA1 decreased in Cisplatin group than that in Control group(all P0.05). The above changes were significantly inhibited in the Cisplatin +Apelin group(all P0.05). Animal experiments showed that the structure of mitochondria in the kidneys of Control group was intact. In the Cisplatin+Saline group, the number of mitochondria decreased significantly, and mitochondrial morphology was distorted with vacuolation. In the Cisplatin+Apelin group, mitochondrial lesions were less severe than those in the Cisplatin+Saline group. Compared with Control group, the levels of plasma Cr, BUN, and urine Kim-1, NGAL were significantly higher in cisplatin +Saline group(all P0.05). However, the above biomarkers in Cisplatin+Apelin group were significantly lower compared with Cisplatin+Saline group(all P0.05). Conclusion Apelin protects the homeostasis of mitochondria by increasing the expression of deacetylase Sirt3, thereby alleviates cisplatin-induced acute kidney injury.
【Fund】: 国家自然科学基金资助项目(81570660);; 北京市医院管理局临床医学发展专项基金资助项目(ZYLX201824);; 首都医科大学科研培育基金资助项目(自然类)(PYZ2018051)
【CateGory Index】: R692
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