| | | 左旋卡尼汀对兔缺血/再灌注心肌细胞凋亡的影响
| | 免费医学论文
作者：马兰香，惠增骞，张华，杨星昌，原平利，段继源，张磊
【关键词】 左旋
Protective effects of carnitine against myocyte apoptosis following myocardial ischemia/reperfusion in rabbits
【Abstract】 AIM: To study the protective effects of carnitine on cardiac myocyte apoptosis following myocardial ischemia/reperfusion (MI/R). METHODS: Rabbits were subjected to 45min myocardial ischemia followed by reperfusion for 3 h. Anesthetized rabbits were randomly divided into 3 group: control group (n=5), in which left anterior descending coronary artery was exposed and a piece of silk thread was placed around the artery but not tied, MI/R group (n=10), in which normal saline 1.5 mL was injected into sublingual vein after MI, and carnitine group (n=10), in which carnitine 1.5 mL/(kg・h) was given intravenously 5 min after MI. The animals were sacrificed and their hearts were harvested. Apoptosis was identified by TUNEL and apoptosis index (AI) was obtained. The expression of Fas and Bcl2 protein was measured by immunohistochemical technique. RESULTS: MI/R caused significant cardiac dysfunction and myocardial death. Compared with the MI/R group, the carnitine group had better protection against MI/R injury, as shown by marked decrease of AI and the average A value of Fas protein, as well as significantly improved the average A value of Bcl2 protein. CONCLUSION: Carnitine can protect myocardium from MI/R injury by modulating the expression of Fas and Bcl2 protein and inhibiting apoptosis following myocardial MI/R.
【Keywords】 carnitine; reperfusion injury; myocardial ischemia; apoptosis
【摘要】 目的免费医学论文
： 观察左旋卡尼汀对心肌缺血/再灌注（MI/R）后心肌细胞凋亡的免费医学论文
影响，探讨其保护作用的机制. 方法： 制备家兔MI/R模型，缺血45 min，再灌注3 h. 25只家兔随机分为三组：对照组（Ⅰ组，n=5），MI/R组(Ⅱ组，n=10), 左旋卡尼汀治疗组（Ⅲ组，n=10）在缺血后5 min 静脉注射左旋卡尼汀［1.5 mL/（kg・h）］. 再灌注结束后检测心肌组织SOD活性，原位末端标记(TUNEL)法测定凋亡心肌细胞，免疫组化法测定凋亡相关基因bcl2, fas的表达. 结果： MI/R造成明显的心脏功能障碍，缺血区细胞凋亡. SOD活性明显升高，凋亡指数（AI）和Fas含量减少（P<0.05）,Bcl2含量明显升高（P<0.05）. 结论：左旋卡尼汀具有抗缺血再灌注后心肌损伤的作用，其机制可能是通过调节Bcl2和Fas介导的细胞凋亡而实现.
【关键词】 左旋卡尼汀；再灌注损伤；心肌缺血；细胞凋亡
0引言
缺血/再灌注（myocardial ischemia/reperfusion，MI/R）损伤是冠状动脉再通后一个重要的并发症，也是致死原因之一. 有学者提出，细胞凋亡可能为再灌注损伤发病机制中的一个重要环节［1］；通过干预凋亡基因的表达以阻断细胞凋亡过程，从而减轻再灌注损伤能否成为防治再灌注损伤的有效方法已受关注. 卡尼汀，又名肉毒碱，可加速脂肪的β氧化，提高三磷酸腺苷（ATP）水平，优化心肌能量代谢途径. 近期的大规模临床试验CEMID的结果提示［2］，左旋卡尼汀明显改善心肌梗死后患者的心功能，降低死亡率，缩小梗死面积. 卡尼汀研究的新发现［3］，提示卡尼汀在对缺血性心脏病的作用中，优化心肌能量代谢，抑制MI/R心肌细胞凋亡可能是保护缺血再灌注心肌的重要机制. 我们通过MI/R模型，探讨左旋卡尼汀对MI/R心肌细胞的保护作用及其可能的机制.
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