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鄧旭坤,付千,舒廣文,鄭燕,徐瑞,邱韻涵,段歡,余惠凡.鞣花酸對順鉑引起小鼠急性腎損傷的影響[J].中南民族大學學報自然科學版,2019,(2):210-214
鞣花酸對順鉑引起小鼠急性腎損傷的影響
Effects of ellagic acid on cisplatin-induced acute kidney injury in mice
  
DOI:10.12130/znmdzk.20190211
中文關鍵詞: 鞣花酸  順鉑  急性腎損傷
英文關鍵詞: ellagic acid  cisplatin  acute kidney injury
基金項目:國家自然科學基金資助項目(81073147);國家科技部“十二五”科技支撐計劃資助項目(2012BAI27B06)
作者單位
鄧旭坤1,付千1,舒廣文1,鄭燕2,徐瑞3,邱韻涵1,段歡1,余惠凡4 1 中南民族大學 藥學院,武漢430074
2 淮北職業技術學院 醫學系
,淮北 235000;3 睢寧縣人民醫院 藥劑科,徐州 221200
4 湖北醫藥學院 武當特色中藥研究湖北省重點實驗室
,十堰 442000 
摘要點擊次數: 195
全文下載次數: 205
中文摘要:
      目的:研究鞣花酸(EA)對順鉑引起小鼠急性腎損傷的減輕作用,探討其可能的機制. 方法:將32只雄性昆明小鼠隨機分為對照組、模型組、EA給藥組(10, 30 mg/kg),給予順鉑(25 mg/kg)建立小鼠急性腎損傷模型,觀察EA給藥后的改善作用.取小鼠血清并用試劑盒測定尿素氮(BUN)、肌酐(Cr)、腫瘤壞死因子α (TNF-α)、白介素1β( IL-1β)和腎組織中總超氧化物歧化酶(T-SOD)、丙二醛(MDA)及還原型谷胱甘肽(GSH)水平.用HE和Tunel染色觀察腎臟病理結構變化和細胞凋亡,用Western blotting測定腎組織中促凋亡蛋白(Bax)和抗凋亡蛋白(Bcl-2)的表達.結果:與模型組比較,EA均能不同程度地降低血清中BUN, SCr, MDA, TNF-α和IL-1β水平,增加腎組織中GSH和T-SOD的活性;下調腎組織中 Bax,上調 Bcl-2 的蛋白表達水平;改善順鉑所致的病理變化.結論:EA對順鉑引起的腎損傷具有保護作用,這與EA的抗氧化、減少炎癥反應和抑制腎小管上皮細胞凋亡有關.
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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