CAJ | 학술논문

目的观察补阳还五汤对小鼠局灶性脑缺血后生长相关蛋白43(GAP-43)和突触素(SYP)表达的影响.方法 36只KM小鼠随机分成假手术组(n=12),模型组(n=12)和补阳还五汤组(n=12).大脑中动脉阻塞(MCAO)30 min诱导小鼠局灶性脑缺血,缺血后24h开始灌服补阳还五汤,每天1次,缺血后第1,3,7,14天分别采用神经症状评分和角实验评价神经功能；缺血后第14天,采用免疫组化检测缺血周边区GAP-43和SYP的表达.结果与模型组比较,补阳还五汤在缺血后第3,7,14天能显著改善神经症状(P＜0.05),第7,14天能显著减少小鼠右转次数(P＜0.05)；脑缺血后14d,模型组GAP-43和SYP平均光密度值分别为0.217 ±0.012,0.278 ±0.019,而补阳还五汤组分别为0.250±0.013,0.323±0.017,两组之间差异有统计学意义(P＜0.01).结论补阳还五汤促进脑缺血后神经功能恢复可能与其促进缺血周边区神经轴突再生和突触可塑性有关.
목적 관찰보양환오탕대소서국조성뇌결혈후생장상관단백43(GAP-43)화돌촉소(SYP)표체적영향.방법 36지KM소서수궤분성가수술조(n=12),모형조(n=12)화보양환오탕조(n=12).대뇌중동맥조새(MCAO)30 min유도소서국조성뇌결혈,결혈후24h개시관복보양환오탕,매천1차,결혈후제1,3,7,14천분별채용신경증상평분화각실험평개신경공능；결혈후제14천,채용면역조화검측결혈주변구GAP-43화SYP적표체.결과 여모형조비교,보양환오탕재결혈후제3,7,14천능현저개선신경증상(P＜0.05),제7,14천능현저감소소서우전차수(P＜0.05)；뇌결혈후14d,모형조GAP-43화SYP평균광밀도치분별위0.217 ±0.012,0.278 ±0.019,이보양환오탕조분별위0.250±0.013,0.323±0.017,량조지간차이유통계학의의(P＜0.01).결론 보양환오탕촉진뇌결혈후신경공능회복가능여기촉진결혈주변구신경축돌재생화돌촉가소성유관.
Objective To investigate the effect of Buyanghuanwu decoction(BYHWD) on the expression of growth-associated protein 43(GAP-43) and synaptophysin(SYP) after focal cerebral ischemia in mice.Methods Focal cerebral ischemia was induced by 30 min of middle cerebral artery occlusion followed by reperfusion.BYHWD (20 g/kg) was administered orally 24 h after ischemia and once a day.The neurological score and the corner test were used to evaluate sensorimotor function on 1,3,7,and 14 days after ischemia.The expression of GAP-43 and SYP in the ischemic boundary zone was determined by immunohistochemistry 14 days after ischemia.Results Compared with the model group,BYHWD significantly ameliorated neurological dysfunction at 3,7 and 14 days and reduced the number of right turn at 7 and 14 days after ischemia(P ＜ 0.05).The average optical density of GAP-43 and SYP was 0.217 ±0.012 and 0.278 ±0.019 at the boundary zone in model group 14 days after ischemia,respectively.BYHWD also significantly increased the immunoreactivity of GAP-43 (0.250 ± 0.013)and SYP(0.323 ± 0.017) (P＜ 0.01).Conclusion BYHWD promotes axonal regeneration and synaptic plasticity in the ischemic boundary zone,which may contribute to functional recovery after focal cerebral ischemia.