【摘要】：目的:探討依達拉奉(EDA)對阿霉素致小鼠心肌損傷的保護作用。方法:以阿霉素3mg/kg腹腔注射,隔日1次,共7次致小鼠心肌損傷,造模同時開始以EDA低、高劑量(5、10mg/kg)連續(xù)2周腹腔注射。光鏡下觀察小鼠心室肌組織形態(tài)學變化;測定血清肌酸激酶(CK)和乳酸脫氫酶(LDH)活性;ELISA法測定反映心肌組織的炎性因子腫瘤壞死因子(TNF-α)和白細胞介素6(IL-6)的水平;比色法檢測心肌組織中的超氧化物歧化酶(SOD)、丙二醛(MDA)和一氧化氮(NO)含量的變化;Western blot檢測心肌組織中轉化生長因子-β1(TGF-β1)和沉默信息調節(jié)因子2的哺乳動物同源體1(SIRT1)蛋白的表達。結果:EDA干預后能減輕阿霉素致心肌損傷小鼠的心肌形態(tài)學損傷,降低心肌酶活性。EDA可減少心肌組織中炎性因子TNF-α和IL-6蛋白的表達,改善小鼠抗氧化應激能力。EDA還能明顯增加阿霉素小鼠心臟SIRT1蛋白表達,并抑制TGF-β1蛋白表達。結論:EDA對阿霉素心肌損傷具有保護作用,其作用機制可能通過調節(jié)SIRT1活性,抑制心臟TGF-β1蛋白表達,并提高機體抗氧化應激能力,從而減少阿霉素對心肌的損害。
[Abstract]:Objective: to investigate the protective effect of Edaravone (EDA) on adriamycin-induced myocardial injury in mice. Methods: adriamycin (3mg/kg) was injected intraperitoneally once every other day for 7 times to induce myocardial injury in mice. At the same time, the model was injected intraperitoneally with low and high dose of EDA (5 ~ 10 mg / kg) for 2 weeks. The changes of myocardium morphology, the activities of serum creatine kinase (CK) and lactate dehydrogenase (LDH), and the levels of inflammatory factor TNF- 偽 and interleukin 6 (IL-6), which reflect myocardial tissue, were observed under light microscope. Changes of (SOD), malondialdehyde (MDA) and nitric oxide (no) (NO) contents in myocardial tissue by colorimetric method; Western blot was used to detect the expression of transforming growth factor 尾 1 (TGF- 尾 1) and mammalian homologue 1 (SIRT1) of silencing signaling factor 2 in myocardial tissue. Results: after intervention of EDA, myocardial morphology and myocardial enzyme activity were reduced in mice with myocardial injury induced by doxorubicin. EDA decreased the expression of TNF- 偽 and IL-6 protein in myocardial tissue. EDA also significantly increased the expression of SIRT1 protein and inhibited the expression of TGF- 尾 1 protein in the heart of adriamycin mice. Conclusion: EDA has protective effect on myocardial injury induced by adriamycin, and its mechanism may be by regulating the activity of SIRT1, inhibiting the expression of TGF- 尾 1 protein in the heart, and increasing the ability of antioxidant stress, thus reducing the myocardial damage caused by doxorubicin.
【作者單位】： 咸寧市第一人民醫(yī)院心內科;
【分類號】：R965

【共引文獻】

相關期刊論文 前2條

1 施盛鋒;朱勁舟;張瑞巖;;晚期糖基化終產(chǎn)物受體在小鼠慢性阿霉素心臟毒性模型中的表達[J];解剖學報;2014年04期

2 鄭嫵媚;王福文;;p38MAPK在心肌損傷中的研究進展[J];食品與藥品;2015年01期

相關博士學位論文 前1條

1 楊怡;硫辛酸活化SIRT1分子改善肝臟脂代謝的機制研究[D];山東大學;2014年

【二級參考文獻】

相關期刊論文 前3條

1 張?zhí)@玲;蘭愛平;鄭東誕;胡芬;郭潤民;沈寧;馮鑒強;廖新學;;依達拉奉保護H9c2心肌細胞對抗化學性低氧引起的損傷[J];中國動脈硬化雜志;2012年04期

2 王睿;徐長慶;;阿霉素心臟毒性作用機制研究進展[J];齊齊哈爾醫(yī)學院學報;2006年10期

3 陳莉娜,臧偉進,唐玉海;白藜蘆醇心血管保護作用研究進展[J];生理科學進展;2003年03期

【相似文獻】

相關期刊論文 前3條

1 劉瑞環(huán);寧澄清;畢艷靜;余聶芳;;SIRT1抑制劑的研究進展[J];中南藥學;2012年08期

2 李燕;崔s，

本文編號：2284071