僵蚕天南星方对大鼠急性缺血性脑水肿MMP-2表达的影响

Effects of Silkworm Arisaema decoction on the expression of Matrix Metalloproteinase 2 in rats with acute ischemic brain edema

目的探讨僵蚕天南星方对大鼠急性缺血性脑水肿基质金属蛋白酶2(MMP-2)表达的影响及其作用机制。方法将SD雄性大鼠随机分为假手术组、模型组、僵蚕天南星方组,除假手术组外,其他2组采用线栓法制备大脑中动脉缺血再灌注模型,采用免疫组织化学法、RT-PCR法观察各组大鼠缺血2 h再灌注24 h、48 h、72 h、96 h大脑皮质中MMP-2的表达情况。结果模型组及僵蚕天南星方组再灌注各时间点MMP-2阳性细胞数明显多于假手术组(P均<0.05),僵蚕天南星方组再灌注各时间点MMP-2阳性细胞数明显少于模型组(P均<0.05);模型组再灌注各时间点MMP-2mRNA表达量均明显高于假手术组(P均<0.05),僵蚕天南星方组再灌注各时间点MMP-2mRNA表达量明显低于模型组(P均<0.05)。结论僵蚕天南星方可能通过抑制MMP-2的表达而减轻脑水肿,改善大鼠缺血性脑损伤。

Objective It is to observe Silkworm Arisaema Decoction on the expression of matrix metalloproteinase 2（ MMP-2） in rats with acute ischemic brain edema and to explore its effect mechanism. Methods The male adult Sprague-Dawley rats were randomly divided into three groups： the sham-operation group,the model group,the Silkworm Arisaema Decoction treatment group. The model of right middle cerebral artery occlusion was established by thread ligation method. The Sprague-Dawley rats received occlusion of the right middle cerebral artery for 2 h,and then reperfusion was made for 24 h,48 h,72 h,96 h respectively. The expressions of MMP- 2 were evaluated by immunohistochemistry and real-time PCR at different time points. Results The expression of MMP- 2 at four different time points in the model group and the Silkworm Arisaema Decoction group were significantly higher than that of the sham group（ P〈0. 01）. Compared with the model group,the expression of MMP- 2 in the Silkworm Arisaema Decoction group at each time point were significantly reduced（ P〈0. 01）. The expression of MMP- 2 mRNA at four different time points in the model group was significantly higher than that of the sham group（ P〈0. 01）. The expression of MMP- 2 mRNA at four different time points in the Silkworm Arisaema Decoction group was less than that of the model group（ P〈0. 01）. Conclusion Silkworm Arisaema Decoction can improve brain tissue damage and reduce brain edema in rats with cerebral ischemia-reperfusion injury,the mechanism might be associated with reducing the expression of MMP- 2.