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目的:观察大鼠局灶性脑缺血损伤后大脑组织COX-2、PGE2、PGJ2的表达及青心酮的干预作用,并对其机制进行初步探讨。方法:SD大鼠随机分为模型组和青心酮(4、12、36mg/kg)4组,改良LONGA法制备脑缺血-再灌注模型,取大脑组织分别采用realtime RT-PCR、ELISA和放射免疫法检测大脑组织中COX-2、NF-κB mRNA和蛋白,PGE2、PGJ2表达。结果:青心酮低剂量能明显降低大脑组织COX-2、NF-κB、PGE2的表达,明显提高PGJ2表达;中、高剂量能显著降低大脑组织COX-2、NF-κB、PGE2的表达,显著提高PGJ2表达。结论:青心酮能降低大鼠局灶性脑缺血损伤后大脑组织COX-2、PGE2的表达,提高PGJ2表达,对大鼠缺血-再灌注损伤有保护作用。其机制可能与抑制NF-κB表达有关。
Objective: To observe the expression of COX-2, PGE2 and PGJ2 in the brain tissue of rats after focal cerebral ischemic injury and the interventional effect of Qingxin Ketone, and to discuss its mechanism. METHODS: Sprague-Dawley rats were randomly divided into 4 groups: the model group and Qingxin Ketone (4, 12, 36 mg/kg). The model of cerebral ischemia-reperfusion was prepared by modified LONGA method. The brain tissues were collected using realtime RT-PCR, ELISA and Radioimmunoassay was used to detect the expression of COX-2, NF-κB mRNA and protein, PGE2 and PGJ2 in the brain tissue. Results: Low dose of Qingxin Ketone can significantly reduce the expression of COX-2, NF-κB and PGE2 in brain tissue and significantly increase the expression of PGJ2. The medium and high doses can significantly reduce the expression of COX-2, NF-κB and PGE2 in brain tissue. Significantly increased PGJ2 expression. Conclusion: Qingxin ketone can reduce the expression of COX-2 and PGE2 in rat brain tissue after focal cerebral ischemic injury, and increase the expression of PGJ2, which has a protective effect on ischemia-reperfusion injury in rats. Its mechanism may be related to the inhibition of NF-κB expression.