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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 investigate the effects of hyperbaric oxygen therapy (HBO) on the expression of RhoA protein and neurological function in the brain of MCAO rats. Methods Totally 126 healthy male Sprague-Dawley rats were randomly divided into sham-operation group, ischemia-reperfusion HBO treatment group (treatment group) and ischemia-reperfusion non-treatment group (control group) Rat middle cerebral artery occlusion (MCAO) model was prepared by thread occlusion, and reperfusion was performed 2h after ischemia. The changes of RhoA protein expression at different time points after modeling in each group were evaluated, and the neurological function scores changed at different time points. Results The expression of RhoA protein was weakly positive in bilateral cerebral cortex and basal ganglia in sham operation group. There was no significant difference in the expression intensity of RhoA at each time point after operation. Compared with the sham operation group, RhoA protein expression of ischemic cortex neurons and glial cells in treatment group and control group began to increase at 6h after ischemia-reperfusion, and the expression of RhoA protein increased progressively with time, After 48h to peak gradually decreased, still significantly increased by the 14th day. The average optical density (AOD) of RhoA positive cells in the two groups at each time point was significantly lower than that in the control group (P <0.01). The treatment group and the control group were compared between the two groups, the treatment group at each time point neurological deficit scores were lower than the control group, to the 14th day after operation, two groups of neurological deficit score was statistically significant (P <0.05). Conclusions (1) There is an increase of RhoA activity in acute and convalescent phase after cerebral ischemia, suggesting that ischemic brain injury initiates the mechanism of endogenous neuro-rehabilitation after injury. (2) HBO treatment can reduce the RhoA protein expression at various time points after cerebral ischemia, consistent with changes in neurological score, suggesting that HBO treatment can regulate RhoA signaling pathway activity, which may be its promotion of brain injury One of the mechanisms of neurological rehabilitation.