CAJ | 학술논문

目的:探讨脑栓康(NSK)对D-半乳糖诱导小鼠脑功能衰退的保护作用. 方法: ICR小鼠随机分为空白对照组、模型对照组、银杏叶提取物(天保宁片)40 mg/kg组、NSK 25 mg/kg组、NSK 50 mg/kg组、 NSK 100 mg/kg组.小鼠每日颈背部皮下注射D-半乳糖 120 mg/kg,采用水迷宫试验,测试小鼠的学习记忆能力,并通过测定模型小鼠的学习记忆能力和脑组织超氧化物歧化酶(SOD),谷胱甘肽过氧化物酶(GSH-Px)活力、丙二醛(MDA)和脂褐素含量,观察 NSK对模型小鼠脑功能衰退的保护作用. 结果: NSK 25,50,100 mg/kg可不同程度地改善模型小鼠的学习能力 [3组小鼠平均到达 B点时间为( 43±18) ,(54±29),(59±61)s;而模型对照组到达 B点时间为(63±26) s,t=2.525～2.731,P< 0.05]和记忆能力 [NSK-25 mg/kg组和模型对照组小鼠平均到达 B点时间为(25±26),(50±35) s, t=2.254,P< 0.05]. 3个剂量均可以增强模型小鼠脑组织 SOD, GSH Px活力,降低 MDA和脂褐素含量( t=-2.675～2.712,P< 0.05, t=-8.806～ 15.989,P< 0.01). 结论:抑制脑组织脂质过氧化反应,提高脑组织的抗氧化能力,可能是 NSK改善行为学异常,防治老年期痴呆的作用机制之一.
목적:탐토뇌전강(NSK)대D-반유당유도소서뇌공능쇠퇴적보호작용. 방법: ICR소서수궤분위공백대조조、모형대조조、은행협제취물(천보저편)40 mg/kg조、NSK 25 mg/kg조、NSK 50 mg/kg조、 NSK 100 mg/kg조.소서매일경배부피하주사D-반유당 120 mg/kg,채용수미궁시험,측시소서적학습기억능력,병통과측정모형소서적학습기억능력화뇌조직초양화물기화매(SOD),곡광감태과양화물매(GSH-Px)활력、병이철(MDA)화지갈소함량,관찰 NSK대모형소서뇌공능쇠퇴적보호작용. 결과: NSK 25,50,100 mg/kg가불동정도지개선모형소서적학습능력 [3조소서평균도체 B점시간위( 43±18) ,(54±29),(59±61)s;이모형대조조도체 B점시간위(63±26) s,t=2.525～2.731,P< 0.05]화기억능력 [NSK-25 mg/kg조화모형대조조소서평균도체 B점시간위(25±26),(50±35) s, t=2.254,P< 0.05]. 3개제량균가이증강모형소서뇌조직 SOD, GSH Px활력,강저 MDA화지갈소함량( t=-2.675～2.712,P< 0.05, t=-8.806～ 15.989,P< 0.01). 결론:억제뇌조직지질과양화반응,제고뇌조직적항양화능력,가능시 NSK개선행위학이상,방치노년기치태적작용궤제지일.
AIM:To study the protective effects of Naoshuankang (NSK) against the cerebral function deterioration in mice induced by D galactose. METHODS:A total of 96 ICR mice were randomly divided into blank control group,model group,Taponing group,and 3 NSK groups with varied NSK doses (25,50 and 100 mg/kg respectively).The model of deteriorated cerebral function was induced by daily subcutaneous injection of D galactose (120 mg/kg) in the mice, and the learning and memory abilities were assessed by water maze test.The protective effects of NSK against the cerebral function deterioration were observed by investigating the changes in learning and memory abilities, cerebral SOD and GSH Px activities, and the levels of MDA and lipofuscin. RESULTS:All three NSK doses could improve the learning and memory abilities to different degrees, with the time of the mice with NSK treatment at 25, 50, 100 mg/kg and of those in model groups to arrive at point B being (43±18),(54±29),(59±61),(63±26) s, respectively,(t=2.525-2.731,P< 0.05).For assessment of the memory ability, the time recorded for the mice in NSK(25 mg/kg) and model groups was (25±26),(50±35) s, respectively (t=2.525-2.731,P<0.05).NSK at the 3 doses could markedly enhance cerebral SOD and GSH Px activities, and decrease the levels of MDA and lipofuscin (t=-2.675- 2.712,P< 0.05,t=- 8.806- 15.989,P<0.01). CONCLUSION:Inhibition of cerebral lipid peroxidation and increase of cerebral anti lipid peroxidation ability may be one of the mechanisms for NSK to ameliorate abnormal behavior in patients and relieve senile dementia.