邓旭坤,付千,舒广文,郑燕,徐瑞,邱韵涵,段欢,余惠凡.鞣花酸对顺铂引起小鼠急性肾损伤的影响[J].中南民族大学学报自然科学版,2019,(2):210-214
鞣花酸对顺铂引起小鼠急性肾损伤的影响
Effects of ellagic acid on cisplatin-induced acute kidney injury in mice
  
DOI:10.12130/znmdzk.20190211
中文关键词: 鞣花酸  顺铂  急性肾损伤
英文关键词: ellagic acid  cisplatin  acute kidney injury
基金项目:国家自然科学基金资助项目(81073147);国家科技部“十二五”科技支撑计划资助项目(2012BAI27B06)
作者单位
邓旭坤1,付千1,舒广文1,郑燕2,徐瑞3,邱韵涵1,段欢1,余惠凡4 1 中南民族大学 药学院武汉430074
2 淮北职业技术学院 医学系
淮北 2350003 睢宁县人民医院 药剂科徐州 221200
4 湖北医药学院 武当特色中药研究湖北省重点实验室
十堰 442000 
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中文摘要:
      目的:研究鞣花酸(EA)对顺铂引起小鼠急性肾损伤的减轻作用,探讨其可能的机制. 方法:将32只雄性昆明小鼠随机分为对照组、模型组、EA给药组(10, 30 mg/kg),给予顺铂(25 mg/kg)建立小鼠急性肾损伤模型,观察EA给药后的改善作用.取小鼠血清并用试剂盒测定尿素氮(BUN)、肌酐(Cr)、肿瘤坏死因子α (TNF-α)、白介素1β( IL-1β)和肾组织中总超氧化物歧化酶(T-SOD)、丙二醛(MDA)及还原型谷胱甘肽(GSH)水平.用HE和Tunel染色观察肾脏病理结构变化和细胞凋亡,用Western blotting测定肾组织中促凋亡蛋白(Bax)和抗凋亡蛋白(Bcl-2)的表达.结果:与模型组比较,EA均能不同程度地降低血清中BUN, SCr, MDA, TNF-α和IL-1β水平,增加肾组织中GSH和T-SOD的活性;下调肾组织中 Bax,上调 Bcl-2 的蛋白表达水平;改善顺铂所致的病理变化.结论:EA对顺铂引起的肾损伤具有保护作用,这与EA的抗氧化、减少炎症反应和抑制肾小管上皮细胞凋亡有关.
英文摘要:
      Objective: To investigate the alleviation effect of ellagic acid (EA) on cisplatin-induced acute kidney injury in mice and to explore the possible mechanism. Methods: 32 male Kunming mice were randomly divided into control group, model group, low and high dose groups (10, 30 mg/kg EA). An acute kidney injury model was established by a single intraperitoneal injection of 25 mg/kg cisplatin to observe the improvement effect after EA administration. Serum urea nitrogen (BUN), creatinine (SCr), tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β) and total superoxide dismutase (T-SOD), malondialdehyde (MDA), and glutathione (GSH) in renal tissues were detected in the serum of each group. Renal pathological changes and apoptosis were observed by HE and Tunel staining. The expressions of proapoptotic protein (Bax) and anti-apoptotic protein (Bcl-2) in renal tissues were determined by Western blotting. Result: Compared with the model group, EA could reduce the levels of BUN, SCr, MDA, TNF-α and IL-1β in serum, increase the activity of GSH and T-SOD in kidney tissue, and down-regulate Bax in kidney tissue and up-regulate Bcl-2 protein expression levels, also improve pathological changes induced by cisplatin. Conclusion: EA has a protective effect on cisplatin-induced renal injury, which may be associated with EA's antioxidant, inflammatory response reduction and inhibition of renal tubular epithelial cell apoptosis.
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