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GSH对乳鼠缺氧/复氧心肌细胞中MDA、IL-1β和TNF-α的影响

Effect of GSH on malondiadehyde,IL-1β and TNF-α in anoxia/re-oxygenation injury of cultured myocardial cells in rats
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摘要 目的:探讨还原型谷胱甘肽(GSH)对缺氧/复氧培养大鼠心肌细胞损伤后MDA、IL-1β和TNF-α的影响。方法:将原代培养的乳鼠心室肌细胞分为对照组、模型组和GSH组,GSH组缺氧、复氧前均给予160mg/L浓度GSH,缺氧2h,复氧1h。复氧1h后,用比色法检测丙二醛(MDA)含量,用RT-PCR法检测细胞内IL-1βmRNA和TNF-αmRNA水平。结果:与对照组相比,模型组MDA水平、IL-1βmRNA和TNF-αmRNA表达显著升高(P<0.01)。GSH预处理可以减轻MDA、IL-1βmRNA和TNF-αmRNA的上调(P<0.01vs模型组)。MDA、IL-1βmRNA和TNF-αmRNA的表达在各组间均呈正相关(P<0.05)。结论:在缺氧/复氧损伤的过程中,炎性细胞因子和氧自由基的作用相互联系,还原型谷胱甘肽能清除氧自由基,抑制IL-1βmRNA和TNF-αmRNA的升高,从而保护缺氧/复氧损伤的心肌细胞。 Objective: To investigate the protective effect of reduced glutathione (GSH) on malond-iadehyde (MDA), interleukin-1β(IL-1β) and tumor necrosis factor-α(TNF-α) in anoxia/reoxygenation injury of myocardial cells in rats. Methods: Primary cultured myocardial cells of rats were randomly allocated into 3 groups: control group, model group and GSH group. The sample of GSH group was given 160mg/L medicament before anoxia and reoxygenation. One hour after reoxygenation, the activity of MDA was detected by colorimetry, and the levels of IL-1βmRNA and TNF-αmRNA were detected by RT-PCR. Results: Compared with the activity of MDA, the expressions of cellular IL-1βmRNA and TNF-αmRNA of control group, those items of model group were significantly increased (P < 0.01). The levels of MDA, IL-1βmRNA and TNF-αmRNA of GSH group were lower than those items of model group (P < 0.01). There were obvious correlations between MDA, IL-1βmRNA and TNF-αmRNA. Conclusion: GSH can protect the myocardial cells from anoxia/reoxygenation injury. It can eliminate the oxidant and reduce the increase of MDA , IL-1βmRNA and TNF-αmRNA. During the development of anoxia/reoxygenation, the function of inflammatory cytokine and the oxygen free radical are correlated with each other.
出处 《山东大学学报(医学版)》 CAS 北大核心 2005年第7期609-611,615,共4页 Journal of Shandong University:Health Sciences
关键词 缺氧/复氧损伤 心肌细胞 谷胱甘肽 白细胞介素1Β 肿瘤坏死因子α Anoxia/reoxygenation injury Myocardial cells Glutathione Interleukin-1β Tumor necrosis factor-α
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