刺五加提取物对大鼠脑缺血再灌注损伤的保护作用

目的研究刺五加提取物(ASE)对大鼠脑缺血再灌注损伤的保护作用。方法将120只大鼠随机分为6组,每组20只,分别为假手术组、模型组、尼莫地平组(15 mg·kg^-1)及ASE高、中、低剂量组(200、100、50 mg·kg^-1),每日1次,连续灌胃给药15 d。采用改良Longa法制备脑缺血再灌注损伤大鼠模型。进行神经功能缺损评分;红四氮唑(TTC)染色后计算脑梗死面积百分比;采用HE染色及TUNEL染色法进行脑组织病理学观察,计算顶叶区皮层及杏仁核区域的细胞凋亡百分率;ELISA法测定脑组织中白介素(IL)-6、IL-1β、肿瘤坏死因子-α(TNF-α)含量;利用试剂盒检测脑组织中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性及丙二醛(MDA)含量。结果与假手术组比较,模型组大鼠的神经功能缺损评分及脑梗死面积百分比显著升高(P<0.001);顶叶皮层和杏仁核处存在大量凋亡细胞;脑组织中的SOD、GSH-Px活性显著降低(P<0.001),MDA、IL-6、IL-1β及TNF-α水平显著升高(P<0.001)。与模型组比较,ASE各剂量组大鼠脑组织中的IL-6、IL-1β含量显著降低(P<0.05,P<0.01);ASE中、高剂量组的神经功能缺损评分、脑梗死面积百分比、脑组织细胞凋亡百分率、MDA水平及TNF-α含量均显著降低(P<0.05,P<0.01),SOD活性显著升高(P<0.05,P<0.01);ASE高剂量组的GSH-Px活性显著升高(P<0.01)。结论 ASE对大鼠脑缺血再灌注损伤具有一定保护作用,其作用机制可能与提高脑组织抗氧化能力,抑制炎症细胞因子过度分泌,以及抑制组织细胞凋亡有关。

Protective Effects of Acanthopanax senticosus Extract on Cerebral Ischemia-reperfusion Injury in Rats

Objective To observe the protective effect of Acanthopanax senticosus extract(ASE) on cerebral ischemiareperfusion injury in Wistar rats.Methods 120 male Wistar rats were randomly divided into Sham group,model(ischemia-reperfusion,I/R) group,Ni modi pine group(15 mg·kg^-1) and ASE dose groups(200,100,50 mg·kg^-1).After 15 days of oral administration in each group,the middle cerebral artery was embolized by modified Longa thread occlusion method to establish the model of cerebral ischemia-reperfusion in rats:ischemia for 2 hours and reperfusion for 24 hours.Finally,the behavioral score,the proportion of cerebral infarction volume,the results of histopathology and the activities of superoxide dismutase(SOD),glutathion peroxidase(GSH-Px),the concentration of malondialdehyde(MDA),Interleukin-6(IL-6) and Interleukin-1 β(IL-1β) in rats’ brains were detected by commercial Kits.Results Compared with the Sham group rats,the behavioral score,the proportion of cerebral infarction volume in model group were significantly increased(P<0.001);activities of SOD and GSH-Px decreased(P<0.001);levels of MDA,IL-6,IL-1β and TNF-α significantly increased(P<0.001).The results of terminal dexynucleotidyl transferase(TdT)-mediated dUTP nick end labeling(TUNEL) showed that,there were a large number of apoptotic cells in the parietal cortex and amygdala in I/R group;and the percentage of apoptosis decreased significantly after treatment.In addition,ASE could also increase the activities of SOD and GSH-Px(P<0.05,P<0.01),decrease the concentration of MDA and the levels of IL-6,IL-1β and TNF-α in the brain of rats with cerebral ischemia-reperfusion injury(P<0.05,P<0.01).Conclusion ASE has a certain protective effect on cerebral ischemia-reperfusion injury,and its mechanism may be related to the improvement of antioxidant capacity of brain tissue,the inhibition of excessive secretion of inflammatory cytokines and the inhibition of apoptosis.