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目的:探讨姜黄素对大鼠心肌梗死(myocardial infarction,MI)后炎症反应的抑制作用及相应机制。方法:采用Wistar大鼠,通过结扎冠状动脉建立MI模型,观察姜黄素对于梗死后不同时间心肌组织中炎症反应和炎症因子表达的影响,探讨其相关的分子生物学机制。结果:与对照组比较,姜黄素的使用明显改善MI后28 d的心脏功能,并降低MI后梗死区1、7、14及28 d的炎症细胞浸润;进一步研究显示姜黄素降低了大鼠MI后不同时段肿瘤坏死因子α、白细胞介素1β和白细胞介素6的表达,并抑制NF-κB和JAK-1/SATA3信号通路的激活。结论:姜黄素可通过抑制MI后炎症相关信号通路的激活来减少梗死区炎症细胞的浸润和炎症因子的分泌,减缓炎症反应,从而起到改善血流动力学、减轻心室重构和维护心功能的保护作用。
Objective: To investigate the inhibitory effect of curcumin on inflammation in rats after myocardial infarction (MI) and its corresponding mechanism. METHODS: Wistar rats were used to establish MI model by ligating the coronary arteries to observe the effect of curcumin on the inflammatory reaction and the expression of inflammatory cytokines in myocardium at different time points after infarction, and to explore its related molecular biological mechanism. RESULTS: Compared with the control group, curcumin significantly improved cardiac function at 28 d after MI and decreased inflammatory cell infiltration at 1, 7, 14 and 28 d after infarction in MI group. Further studies showed that curcumin reduced MI TNFα, IL-1β and IL-6 at different time points and inhibited the activation of NF-κB and JAK-1 / SATA3 signaling pathway. CONCLUSION: Curcumin can reduce the infiltration of inflammatory cells and the secretion of inflammatory cytokines in infracted areas by inhibiting the activation of inflammation-related signaling pathways and relieve the inflammatory reaction, thereby improving hemodynamics, reducing ventricular remodeling and maintaining cardiac function The protective effect.