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TNFα、IL-1β模拟心肌缺氧预处理的实验研究 被引量:1

Mimic hypoxia preconditioning on myocardiocytes by TNFα and IL-1β
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摘要 目的 证实用低剂量白细胞介素 1β(Interleukin 1β ,IL 1β)和肿瘤坏死因子α(Tumornecrosisfactoralpha ,TNFα)模拟缺血预处理 (Preconditioning ,PC)能否诱导心肌延迟保护 (Delayedprotection ,DP) ,并探讨其机制。方法 在大鼠培养心肌细胞缺氧复氧模型上 ,观察IL 1β和 /或TNFα预处理后即刻和 2 4h热休克蛋白 72 (Heatshockprotein 72 ,HSP72 )、超氧化物歧化酶 (Superoxidedismutase ,SOD)、丙二醛 (Malonadehyde ,MDA)、谷胱甘肽 (Glutathion ,GSH)和细胞内游离钙 [Ca2 + ]i浓度的变化 ,并测定细胞存活率。结果 与正常对照组 (Control)和缺氧复氧组 (A/R)比较 ,IL 1β预处理 (ILPC)和TNFα预处理 (TNFPC)后 2 4hA/R末 ,HSP72表达和SOD含量显著增加 (P <0 .0 1) ,GSH、细胞存活率有不同程度减少 ,而MDA、[Ca2 + ]i有不同程度增加 ,但分别较A/R组降幅和增幅小 (P <0 .0 5 )。PC后即刻各组间比较差异无显著性 (P >0 .0 5 )。结论 低剂量IL 1β和 /或TNFα预处理心肌细胞可诱导DP ,其机制与心肌细胞氧化 抗氧化平衡和保护蛋白增加有关。 Objective To investigate whether mimic preconditioning (PC) by IL 1β and TNFα treatment at low concentration can induce the delayed protection of myocardium and explore the mechanism. Methods After the myocardiocytes were cultured under normal, anoxia/reoxygenation (A/R) conditions or with TNFα or IL 1β pretreatment, the expression of heat shock protein 72 (HSP72), the contents of superoxide dismutase (SOD), glutathion (GSH), malonadehyde (MDA) and the concentration of intracellular dissociative calcium ([Ca 2+ ]i) in the cells were measured with immunohistochemical and enzyme methods just after the pretreatment or 24 h later. The survival rate of the cultured cardiac myocytes was determined. Results In the cells with TNFα or IL 1 β pretreatment for 24 h, at the end of A/R culture the expression of HSP72 and the content of SOD were increased significantly in comparison with those in control and A/R groups, and the GSH content and cell survival rate were reduced, but the MDA content and [Ca 2+ ]i concentration were elevated to some extents, with the increased and decreased amplitudes lower than those of A/R group ( P <0.05). No significant difference was found among the groups immediate after culture. Conclusion Low IL 1β and/or TNFα pretreatment can induce the late cardioprotection and its mechanism is associated with the increase of protectiiv proteins and the balance of oxidants and antioxidants.
出处 《第三军医大学学报》 CAS CSCD 北大核心 2001年第7期777-779,共3页 Journal of Third Military Medical University
关键词 白细胞介素-1Β 肿瘤坏死因子 预处理 延迟保护 心肌缺氧 interleukin 1β tumor necrosis factor preconditioning delayed protection
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