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作 者:刘玉莲 巫芳华 杨开令 周颖 周乐全[1] 刘微[1] LIU Yu-lian;WU Fang-hua;YANG Kai-ling;ZHOU Ying;ZHOU Le-quan;LIU Wei(Basic Medical College,Guangzhou University of Chinese Medicine,Guangzhou,Guangdong 510006,China)
机构地区:[1]广州中医药大学基础医学院,广东广州510006
出 处:《时珍国医国药》2021年第6期1304-1307,共4页Lishizhen Medicine and Materia Medica Research
基 金:国家自然科学基金(81673772);广州中医药大学“青年英才培养工程”项目(QNYC20170102)。
摘 要:目的探讨FPR2在补阳还五汤减轻大鼠脑缺血再灌注中作用。方法运用线栓法建立大脑中动脉栓塞(MCAO)模型。实验动物随机分为假手术组、模型组、补阳还五汤组和补阳还五汤联合FPR2抑制剂(Boc-2)组。补阳还五汤剂量为每次16 g/kg,每天灌胃2次,术前30 min腹腔注射Boc-2(0.4 mg/kg),缺血后6 h,24 h,2 d,3 d,7 d,运用Western blot检测FPR2蛋白表达和ELISA检测FPR2内源性配体LXA4和RvD1蛋白表达;缺血后24 h进行平衡木和抓力评分,以及测定脑梗死面积。结果与模型组比,补阳还五汤组FPR2和RvD1在缺血后24 h达到高峰(P<0.05);据此,选择缺血后24 h为后续实验时间点,发现补阳还五汤能改善大鼠平衡功能、抓力和减小脑梗死面积(P<0.01,P<0.05);但联合使用Boc-2后,大鼠行为学功能下降和脑梗死面积增加(P<0.01,P<0.05)。结论补阳还五汤可能通过增强FPR2作用减轻大鼠脑缺血再灌注神经功能损伤、减少脑梗死面积,从而发挥保护作用。Objective To investigate the role of FPR2 in protective effects of Buyang Huanwu Decoction on the Cerebral Ischemia Reperfusion Injury in Rats.Methods The middle cerebral artery occlusion(MCAO)model was established by Longa method.The rats after MCAO were randomly divided into:sham operation group,model group,BYHWD group,BYHWD+Boc-2(FPR2 antagonist)group,the dose of BYHWD was 16 g/kg each time and given twice a day,Boc-2 was injected intraperitoneally(0.4 mg/kg)30 minutes before surgery.Time course expressions of FPR2,and RvD1 were detected by Western blot and ELISA respectively at 6 h,24 h,2 d,3 d,7 d post ischemia-reperfusion.24 h after surgery.The neurological performance was evaluated by beam-walking test and Grip Strength experiment.TTC was conducted for infarct area.Results Compared with MCAO group,BYHWD enhanced the expressions of FPR2,LXA4,and RvD1,peaking at 24 h(P<0.05).Thus 24 h was chosen to be the observation time point for the following experiments.Compared with MCAO group,it was found that BYHWD improved neurological behavior(indicated by beam-walking test and Grip Strength test)and decreased the cerebral infarct area(P<0.01,P<0.05).However,the effects of BYHWD was partly inhibited by coadiministration with Boc-2(P<0.01,P<0.05).Conclusion These findings suggested that FPR2 was involved in the protective role of BYHWD in promoting neural function recovery and reducing cerebral infarct area after ischemic-reperfusion injury.
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