灯盏花素；巴马小型猪；脑死亡；心脏；蛋白激酶C_

灯盏花素对脑死亡巴马小型猪心脏结构、功能及蛋白激酶C表达的影响

http://www.100md.com 《西安交通大学学报》 2007年第1期

灯盏花素；巴马小型猪；脑死亡；心脏；蛋白激酶C,,灯盏花素；巴马小型猪；脑死亡；心脏；蛋白激酶C,1材料与方法,2结果,3讨论,参考文献：

     摘要：目的探讨灯盏花素对脑死亡巴马小型猪心脏结构、功能及蛋白激酶C(protein kinase C, PKC)表达的影响。方法巴马小型猪15只，随机分为脑死亡组、灯盏花素组及对照组。应用缓慢间断颅内加压法建立脑死亡模型。分别于脑死亡后6、12和24h取血清及心肌组织进行研究。结果 ①脑死亡24h灯盏花素组心肌损伤明显轻于脑死亡组；②脑死亡后各时间点灯盏花素组血清肌钙蛋白T(cTnT)、白介素1β(IL1β)、白介素6(IL6)、肿瘤坏死因子α(TNFα)水平均较脑死亡组低；③脑死亡24h灯盏花素组心肌蛋白激酶C表达水平均显著低于脑死亡组。结论灯盏花素可通过抑制蛋白激酶C，减少炎症因子释放，减轻脑死亡巴马小型猪的心脏损伤。

    关键词：灯盏花素；巴马小型猪；脑死亡；心脏；蛋白激酶C

    Effects of breviscapine on the heart structure and function and PKCα expression in braindead BAMa minipigs

    Zhu Changju, Lu Xu, Zhu Shengxing, Zhao Yongfu, Ma Xiuxian, Zhang Shuijun

    (Emergency Department; Surgery Department, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China)

    ABSTRACT: Objective To investigate the effects of breviscapine on the heart structure and function and PKCα mRNA and its protein expression in braindead BAMa minipigs. Methods Fifteen BAMa minipigs were randomized into 3 groups: braindead group, breviscapine group, and control group, with 5 pigs in each group. The braindead models were established by increasing intracranial pressure slowly and intermittently, while the animals in control group were maintained anesthesia for 24h. At 6, 12 and 24h after the initial brain death, serum troponinT, TNFα, IL1β, and IL6 were determined. At 24h, heart tissues were taken, the changes of heart tissues were observed by HE staining and the ultrastructural changes of heart cells were observed under electron microscope. The expression of PKCα was detected by immunohistochemistry, and PKCα mRNA was detected by RTPCR. Results ① Morphological changes of heart cells: Changes of heart cells could be found, the degree of heart cell injury in breviscapine pretreatment group was less severe than that in braindead group. ② Serum troponinT in braindead group and breviscapine pretreatment braindead group began to increase gradually since 6h after brain death; troponinT in braindead group was higher at each time point compared with that in breviscapine pretreatment group (P<0.05). ③ Changes of inflammatory factors: Since 6h after the initial brain death, IL1β, IL6, and TNFα in braindead group and breviscapine pretreatment group began to increase and became higher gradually. Compared with those in breviscapine pretreatment group, these inflammatory factors in braindead group were significantly higher at each time point (P<0.05). ④ Changes of PKCα mRNA and protein expression in heart cells: PKCα mRNA and protein expression in braindead group and breviscapine pretreatment group increased at 24h compared with control group; it was significantly higher in braindead group than in breviscapine pretreatment group (P<0.05). Conclusion Breviscapine can inhibit the degree of PKCα mRNA transcription and protein translation, decrease the release of inflammatory factors, and then alleviate heart injury during brain death. ......

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