阿托伐他汀对冠状动脉微栓塞后非梗死区心肌炎症的影响 |
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引用本文: | 李淑梅,刘永平,黄章敏,等. 阿托伐他汀对冠状动脉微栓塞后非梗死区心肌炎症的影响[J]. 心脏杂志, 2013, 25(5): 509-511 |
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作者姓名: | 李淑梅 刘永平 黄章敏 等 |
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作者单位: | (南京军区福州总院476医院心内科,福建 福州 350001) |
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基金项目: | 南京军区医学科技创新基金项目资助(09MA104) |
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摘 要: | 目的:探讨阿托伐他汀干预治疗对冠状动脉微栓塞(CME)后非梗死区心肌炎症的影响。方法: 给清洁级雄性新西兰兔选择性经左前降支(LAD)注入微栓子颗粒悬液建立CME模型,将36只新西兰兔随机分为CME组(模型组)、阿托伐他汀(atrovastatin)干预组及对照组,每组12只(n=12)。于术后7 d处死,取左心室乳头段心肌经HE染色后,观察梗死心肌并检测梗死面积。用ELISA法及RT-PCR检测肿瘤坏死因子α(TNF-α)、白介素6(IL-6)及其基因在非梗死区(右室)心肌中的表达。结果: 前降支动脉微栓塞后,非梗死区右室心肌中白细胞浸润明显增多,TNF-α、IL-6蛋白及其基因的表达显著增强。与未处理组相比,阿托伐他汀可显著抑制CME后右室心肌中白细胞浸润及TNF-α、IL-6蛋白及其基因的表达(均P<0.01)。结论: 冠脉微栓塞后,炎症反应的激活不仅局限于梗死灶,且累及非梗死区心肌。阿托伐他汀可显著抑制CME后非梗死区心肌炎症反应。
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关 键 词: | 阿托伐他汀 冠状动脉 栓塞 炎症反应 兔 |
收稿时间: | 2013-03-25 |
Roles of atorvastatin in myocardial inflammation of uninfarcted area following coronary microembolization |
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Abstract: | AIM:To investigate the roles of atorvastatin in myocardial inflammation of uninfarcted area following coronary microembolization (CME). METHODS: CME model in rabbits was established by injecting homologous microthrombotic particle suspension into the left descending anterior branch (LAD). Thirty-six New Zealand rabbits were randomized to untreated CME group, atorvastatin-treated CME group and sham operation group (n=12/group). Rabbits were sacrificed on postoperative day 7. The morphological characteristics were evaluated in sections with H/E staining and protein and gene expressions of TNFα and IL-6 were semiquantitatively analyzed by ELISA and RT-PCR. RESULTS: LAD microembolization produced increased leukocyte infiltration and strong TNFα, IL-6 mRNA and protein expressions in uninfarcted right ventricular myocardium. Atorvastatin significantly suppressed the inflammatory cell infiltration and protein and gene expression of TNFα and IL-6 (P<0.01). CONCLUSION: Coronary microembolization produces myocardial inflammatory activation, which is not only confined to the microinfarcted zones but also the uninfarcted area. Atorvastatin markedly suppresses TNFα, IL-6 protein and gene expressions and effectively ameliorates myocardial inflammation in the uninfarcted area. |
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