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目的研究肌苷对大鼠脑缺血再灌注后COX-2 mRNA及其蛋白表达影响,探讨其神经保护作用机制。方法应用线栓法建立大鼠脑缺血再灌注动物模型,肌苷组缺血再灌注前腹腔注射肌苷(100 mg/kg),假手术组和对照组同步注射相同剂量生理盐水。原位杂交法和免疫组织化学法检测大鼠脑缺血再灌注后COX-2 mRNA及蛋白的表达。结果对照组皮质和纹状体区COX-2 mRNA表达于脑缺血再灌注6 h开始增强,12 h达高峰,持续1~3 d,然后逐渐降低,至14 d仍高于再灌注2 h水平,同一时间点皮质区高于纹状体区。肌苷组COX-2 mRNA表达于脑缺血再灌注2 h~14 d较对照组显著减低(t=5.50~11.66,P<0.01)。对照组皮质和纹状体区COX-2蛋白表达的变化趋势与COX-2 mRNA相似,但其高峰出现在24 h,较COX-2 mRNA略延迟,且持续时间短,至7 d已降至再灌注2 h水平,同一时间点皮质区高于纹状体区。肌苷组COX-2表达于脑缺血再灌注2 h~14 d较对照组显著减低(t=3.27~18.14,P<0.01)。结论肌苷对脑缺血的保护作用可能是通过下调COX-2 mRNA及蛋白表达而实现的。
Objective To study the effect of inosine on the expression of COX-2 mRNA and its protein after cerebral ischemia-reperfusion in rats and its neuroprotective mechanism. Methods The rat model of cerebral ischemia / reperfusion was established by thread occlusion. Inosine (100 mg / kg) was intraperitoneally injected into the inosine group and the same dose of saline was injected into the sham operation group and the control group simultaneously. In situ hybridization and immunohistochemistry were used to detect the expression of COX-2 mRNA and protein after cerebral ischemia-reperfusion in rats. Results The expression of COX-2 mRNA in cortex and striatum of control group began to increase at 6 h after cerebral ischemia-reperfusion, peaked at 12 h and continued for 1-3 d, then decreased gradually to 14 d after reperfusion for 2 h Level, at the same time cortex area higher than the striatum area. The COX-2 mRNA expression in inosine group was significantly decreased from 2 h to 14 d after cerebral ischemia-reperfusion (t = 5.50 ~ 11.66, P <0.01). COX-2 protein expression in the cortex and striatum of the control group showed a trend similar to that of COX-2 mRNA but peaked at 24 h, slightly delayed compared with COX-2 mRNA and lasted for a short time and dropped to the level of 7 d At 2 h after reperfusion, the cortical area was higher than the striatum at the same time point. The COX-2 expression in inosine group was significantly lower than that in control group at 2 h to 14 d after cerebral ischemia-reperfusion (t = 3.27-18.14, P <0.01). Conclusion Inosine has a protective effect on cerebral ischemia by down-regulating the expression of COX-2 mRNA and protein.