CAJ | 학술논문

目的探讨红景天苷原料药对全脑缺血再灌注大鼠脑水肿和神经功能的影响.方法 100只Sp rague-Dawley大鼠随机分为假手术组、缺血再灌注组以及红景天苷12、24和48 mg/kg组,每组20只；各组再分为6h、24 h、72 h和7 d组,每组5只.四血管闭塞法建立大鼠全脑缺血模型.各组均在模型制作后即刻开始灌胃给药,连续7d.干湿重法检测脑水含量.采用神经功能缺损量表(neurologic deficit score,NDS)评价神经功能.结果缺血再灌注组和红景天苷组在模型制作后均出现显著的神经功能缺损,并随着时间推移逐渐减轻.各红景天苷组神经功能缺损均较相应时间点缺血再灌注组显著改善(P均＜0.05),且呈剂量依赖趋势；模型制作后72 h和7d时红景天苷48 mg/kg组神经功能缺损较红景天苷12 mg/kg组和24 mg/kg组显著改善(P均＜0.05).缺血再灌注组和红景天苷组脑含水量均在制模后6h开始升高,72 h时达高峰,显著高于假手术组(P均＜0.05).红景天苷组在模型制作后24 h和72 h时脑含水量显著低于缺血再灌注组(P均＜0.05),呈剂量依赖趋势,到模型制作后7d时,红景天苷48 mg/kg组脑含水量已接近假手术组.结论红景天苷能显著减轻全脑缺血再灌注大鼠脑水肿和改善神经功能,具有神经保护作用.
목적 탐토홍경천감원료약대전뇌결혈재관주대서뇌수종화신경공능적영향.방법 100지Sp rague-Dawley대서수궤분위가수술조、결혈재관주조이급홍경천감12、24화48 mg/kg조,매조20지；각조재분위6h、24 h、72 h화7 d조,매조5지.사혈관폐새법건립대서전뇌결혈모형.각조균재모형제작후즉각개시관위급약,련속7d.간습중법검측뇌수함량.채용신경공능결손량표(neurologic deficit score,NDS)평개신경공능.결과 결혈재관주조화홍경천감조재모형제작후균출현현저적신경공능결손,병수착시간추이축점감경.각홍경천감조신경공능결손균교상응시간점결혈재관주조현저개선(P균＜0.05),차정제량의뢰추세；모형제작후72 h화7d시홍경천감48 mg/kg조신경공능결손교홍경천감12 mg/kg조화24 mg/kg조현저개선(P균＜0.05).결혈재관주조화홍경천감조뇌함수량균재제모후6h개시승고,72 h시체고봉,현저고우가수술조(P균＜0.05).홍경천감조재모형제작후24 h화72 h시뇌함수량현저저우결혈재관주조(P균＜0.05),정제량의뢰추세,도모형제작후7d시,홍경천감48 mg/kg조뇌함수량이접근가수술조.결론 홍경천감능현저감경전뇌결혈재관주대서뇌수종화개선신경공능,구유신경보호작용.
Objective To investigate the effect of salidroside on brain edema and neurological function in global cerebral ischemia-reperfusion injury in rats.Methods A total of 100 Sprague Dawley rats were randomly divided into sham operation,ischemia-reperfusion and salidroside 12,24 and 48 mg/kg groups (n =20 in each group),and than redivided into 6 h,24 h,72 h and 7 dsubgroups (n =5 in each subgroup).A rat model of global cerebral ischemia was established using the four-vessel occlusion method.Immediately after modeling,all groups were administered intragastrically for 7 days.The brain water content was quantitated by the wet-dry weight method.The neurological evaluation was performed using a neurological deficit score (NDS).Results After modeling both the ischemia-reperfusion group and all the salidroside groups had significant neurological deficit,and as time went by,it was improved gradually.Compared to the ischemia-reperfusion group at the corresponding time points,neurological deficit in all the salidroside groups was improved significantly (all P ＜ 0.05),and showing a dose-dependent trend.Compared to the salidroside 12 mg/kg and 24 mg/kg groups,neurological deficit in the salidroside 48 mg/kg group was improved significantly at 72 hours and 7 days (all P ＜ 0.05).The brain water contents began to increase at 6 hours after modeling in the the ischemia-reperfusion group and all the salidroside group.They reached the peak at 72 hours,and significantly higher than that in the sham operation group (all P ＜ 0.05).The brain water contents in all the salidroside group were significantly lower than those in the ischemiareperfusion group at 24 and 72 hours after modeling (all P ＜ 0.05) and showing a dosedependent trend.The brain water content in the salidroside 48 mg/kg group was close to that in the sham operation group at 7 days after modeling.Conclusions Salidroside may significantly decrease brain edema and improve neurological function in global cerebral ischemia-reperfusion injury in rats,and it has a neuroprotective effect.