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目的采用颈交感干离断(transection of cervical sympathetic trunk,TCST)方法模拟星状神经节阻滞(stellateganglion block,SGB),观察其对局灶性脑缺血再灌注损伤大鼠皮质区神经元凋亡以及内质网应激相关因子GRP78和CHOP表达的影响。方法健康雄性SD大鼠150只,按随机数字表法分成3组:假手术组(sham组)、再灌注模型组(I/R组)、治疗组(T组),每组50只。用线栓法行大脑中动脉栓塞(MCAO)建立大鼠局灶性脑缺血再灌注损伤模型。治疗组行大脑中动脉栓塞后立即行TCST。应用免疫组化及实时荧光定量PCR方法检测脑缺血再灌注后不同时间点缺血周围区GRP78和CHOP的表达;TUNEL法检测细胞凋亡。结果 I/R组和T组皮质区神经元凋亡指数较sham组显著增高(P<0.01);与I/R组相比,T组再灌注12、24、48、72h凋亡指数明显降低(P<0.05,P<0.01)。I/R组和T组GRP78、CHOPmRNA和蛋白表达较sham组明显上调(P<0.01);与I/R组相比,除72h外,T组6、12、24、48h GRP78、CHOP mRNA和蛋白的表达量明显降低(P<0.05,P<0.01),但仍高于sham组(P<0.05)。结论 TCST对大鼠局灶性脑缺血损伤具有保护作用,其作用机制可能与改善内质网应激状态、降低内质网应激相关凋亡途径,从而发挥抗凋亡作用有关。
Objective To observe the effect of transection of cervical sympathetic trunk (TCST) on stellate ganglion block (SGB) in the cortex of rats with focal cerebral ischemia-reperfusion injury Effects of Endoplasmic Reticulum Stress Related Factors GRP78 and CHOP Expression. Methods 150 healthy male Sprague-Dawley rats were divided into 3 groups according to the random number table: Sham group, I / R group and T group. Establishment of a rat focal cerebral ischemia / reperfusion injury model by middle cerebral artery occlusion (MCAO). The treatment group received immediate middle cerebral artery occlusion (TCST). The expression of GRP78 and CHOP at different time points after cerebral ischemia-reperfusion was detected by immunohistochemistry and real-time fluorescence quantitative PCR. Apoptosis was detected by TUNEL. Results Compared with sham group, the apoptosis index of cortex in I / R group and T group was significantly higher than that in sham group (P <0.01). Compared with I / R group, apoptotic index of T group at 12, 24, 48 and 72 h after reperfusion was significantly lower (P <0.05, P <0.01). Compared with I / R group, the expression of GRP78, CHOP mRNA and protein of I / R group and T group were significantly up-regulated compared with sham group (P <0.01) The protein expression was significantly decreased (P <0.05, P <0.01), but still higher than sham group (P <0.05). Conclusion TCST has a protective effect on focal cerebral ischemic injury in rats. Its mechanism may be related to the improvement of endoplasmic reticulum stress state, the decrease of endoplasmic reticulum stress-related apoptotic pathway and the anti-apoptotic effect.