机构地区:[1]重庆三峡中心医院神经内科,重庆404000 [2]重庆医科大学附属第二医院神经内科 [3]第三军医大学西南医院神经内科
出 处:《中华物理医学与康复杂志》2007年第9期577-580,共4页Chinese Journal of Physical Medicine and Rehabilitation
摘 要:目的探讨高压氧(HBO)治疗对MCAO大鼠脑组织RhoA蛋白的表达强度变化和神经功能评分的影响。方法将126只健康的雄性SD大鼠随机分为假手术组、缺血2h再灌注HBO治疗组(治疗组)和缺血再灌注未作处理组(对照组),每组大鼠42只。用线栓法制备大鼠大脑中动脉闭塞(MCAO)模型,缺血2h后再灌注。评定各组脑组织造模后不同时间点RhoA蛋白的表达变化、不同的时间点神经功能评分改变。结果假手术组双侧大脑皮质和基底节区可见RhoA蛋白弱阳性表达,术后各时间点表达强度无明显差异。与假手术组比较,治疗组和对照组缺血侧皮质神经元细胞和神经胶质细胞RhoA蛋白表达在缺血再灌注后6h开始增加,随着时间的延长,RhoA蛋白的表达进行性增加,至48h达到高峰之后逐渐下降,到第14天仍明显增高。治疗组和对照组两组各时点RhoA蛋白阳性细胞平均光密度(AOD)比较差异有统计学意义(P<0.01)。治疗组和对照组两组间比较,治疗组各时间点神经功能缺损评分均低于对照组,到术后第14天时,2组神经功能缺损评分有统计学意义(P<0.05)。结论(1)脑缺血后急性期和恢复期存在RhoA活动的增强,提示缺血性脑损伤启动了内源性抑制损伤后神经功能康复的机制。(2)HBO治疗可降低RhoA蛋白在脑缺血后各时间点的阳性表达,和神经功能评分改变相一致,提示HBO治疗有调节RhoA信号传导通路活动的作用,这可能是其促进脑损伤后神经功能康复的机制之一。Objective To evaluated the effect of hyperbaric oxygenation therapy (HBO) on the RhoA expression and nerve function after transient focal cerebral ischemia in a rat model of middle cerebral artery occlusion. Methods One hundred and twenty-six healthy Sprague-Dawley rats were used and randomly divided into a sham operation group (shame group, n=42), atreatment group (n=42), and a control group (n=42). The animal model of middle cerebral artery occlusion (MCAO) was established by using the Zea-Longa method with the animals in the treatment and the control groups, and sham operation was performed with those in the sham group. HBO was applied to the animals in the treatment group. The RhoA protein expression was observed by using immunohistochemistry technique, and the neurological function was evaluated by Bederson's scale at different time points after MCAO. Resuits ( Ⅰ ) Weakly positive expression of RhoA could be located in bilateral cortex and the basal ganglia in the sham group. The expression of RhoA in the treatment group and control group was increased as early as 6 hours after MCAO when compared with that of the sham group, and peaked at 48 h after MCAO and decreased after then, but was still higher than that of the shame group at 7th day to 14th day after MCAO. It was also found that the expression of RhoA of the treatment group was significantly lower than that of the control group ( P 〈 0. 01 ). ( 2 ) Evaluation with Bedersons's scale showed that the neurological function of treatment group was significantly better than the control group( P 〈 0.05 ). Conclusion ( 1 ) The expression of RhoA was enhanced in the acute and recovery stages of cerebral infarction, which suggested that the endogenic mechanism activated by cerebral ischemic injury had inhibited neurological function rehabilitation. (2) HBO could reduce the expression of RhoA protein after cerebral isehemia, which was parallel to the change of neurological function, suggesting that the rehabil
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