CAJ | 학술논문

目的：探讨左归丸对慢性脑缺血线粒体呼吸链酶复合物活性的影响及其机制。方法将实验大鼠随机分为对照组、假手术组、慢性脑缺血组和左归丸治疗组，各8例。后两组大鼠采用双侧颈总动脉结扎法建立慢性脑缺血大鼠模型。左归丸治疗组于术后3周开始每天予以左归丸液灌胃，剂量为4.0 g/kg/d。术后6周，测试各组大鼠脑皮质线粒体活性氧（ ROS）水平及线粒体呼吸链酶复合物活性测定。结果与对照组及假手术组比较，慢性脑缺血组大鼠的脑的线粒体ROS水平明显增高（ P＜0.01），呼吸链酶复合物Ⅰ-Ⅳ活性均有不同程度的明显降低（P＜0.01）；接受左归丸治疗组的大鼠的脑的线粒体ROS水平明显降低（P＜0.05），呼吸链酶复合物Ⅳ（COX）活性得到明显改善（P＜0.05）。结论左归丸可能通过修复线粒体COX的活性水平，改善线粒体功能，减少ROS的生成，从而起到对慢性缺血的保护作用。
목적：탐토좌귀환대만성뇌결혈선립체호흡련매복합물활성적영향급기궤제。방법장실험대서수궤분위대조조、가수술조、만성뇌결혈조화좌귀환치료조，각8례。후량조대서채용쌍측경총동맥결찰법건립만성뇌결혈대서모형。좌귀환치료조우술후3주개시매천여이좌귀환액관위，제량위4.0 g/kg/d。술후6주，측시각조대서뇌피질선립체활성양（ ROS）수평급선립체호흡련매복합물활성측정。결과여대조조급가수술조비교，만성뇌결혈조대서적뇌적선립체ROS수평명현증고（ P＜0.01），호흡련매복합물Ⅰ-Ⅳ활성균유불동정도적명현강저（P＜0.01）；접수좌귀환치료조적대서적뇌적선립체ROS수평명현강저（P＜0.05），호흡련매복합물Ⅳ（COX）활성득도명현개선（P＜0.05）。결론좌귀환가능통과수복선립체COX적활성수평，개선선립체공능，감소ROS적생성，종이기도대만성결혈적보호작용。
Objective To investigate the effects of Zuogui Pill on the activities of mitochondrial respiratory chain in rats with chronic cerebral ischemia . Methods Rats were divided into the control group , the sham operation group, the chronic cerebral ischemia group and the Zuogui Pill treatment group , as each group had 8 rats.Rats in the later two groups were subjected to permanent bilateral common carotid artery occlusion .Three weeks after operation , Zuogui Pill was given orally by gavage to Zuogui Pill treatment group rats at doses of 4.0 g/kg/d.Six weeks after operation, reactive oxygen species ( ROS) production and the enzyme activities of mitochondrial respiratory chain complexes in rats from each group were monitored . Results Compared with the rats in the control group and the sham-operation group , rats in the chronic cerebral ischemia group had higher ROS level ( P<0.05 ) and decreased levels of the activities of respiratory chain complexesⅠ-Ⅳ.Compared with that in the chronic cerebral ischemia group, the rats in the Zuogui Pill treatment group had obviously decreased ROS level and significantly increased activity of respiratory chain complex IV (COX) (P<0.05). Conclusion Zuogui Pill can increase the activity of mitochondrial COX and decrease the elevated level of ROS caused by chronic ischemia which may be one of the possible mechanisms of its protective action against chronic cerebral ischemia .