论文部分内容阅读
目的 :探讨丹栀逍遥散 (DZXYS)防治D 半乳糖 (D galactose ,D gal)致拟阿尔茨海默病 (AD)模型的作用机制。 方法 :大鼠皮下注射D gal 15 0mg/ (kg·d)× 4 9d造模 ,以0 .5 4mg/ (kg·d)盐酸多奈哌齐为阳性对照药物 ,用12 .6 4 g/ (kg·d)DZXYS同步灌胃给药防治模型损伤。第 4 2～ 4 6天进行水迷宫实验和跳台实验 ;第 5 0天处死大鼠取脑组织 ,生物化学方法检测脑组织超氧化歧化酶 (SOD)活性和脂质过氧化物 (MDA)含量。结果 :①DZXYS提高AD大鼠主动学习记忆成绩的疗效优于盐酸多奈哌齐。②DZXYS恢复AD大鼠被动学习记忆成绩的疗效相当于盐酸多奈哌齐。③DZXYS使造模大鼠大脑SOD活性从 35 2 .6 7± 37.71回升到 (380 .73± 14 .85 )u/mg pr(P <0 .0 5 )。④DZXYS使造模大鼠大脑MDA含量从 7.88± 0 .70回降到 (6 .6 4± 0 .80 )ng/mg pr(P <0 .0 1)。结论 :减轻自由基损害是DZXYS防治拟AD模型动物的主要机制之一。
Objective : To investigate the mechanism of DZXYS in preventing and treating Alzheimer’s disease (AD) model induced by D galactose (D gal). METHODS: Rats were injected subcutaneously with D gal 150 mg/(kg·d)×4 9 days, and 0.54 mg/(kg·d) of donepezil hydrochloride as a positive control drug, with 12.64 g/(kg· d) DZXYS simultaneous gavage administration prevents model damage. The water maze test and the step-down experiment were conducted from day 42 to day 46. The brains were sacrificed on the 50th day. The superoxide dismutase (SOD) activity and lipid peroxide (MDA) content in brain tissue were detected by biochemical methods. . Results: 1DZXYS was superior to donepezil hydrochloride in improving the active learning and memory performance of AD rats. The efficacy of 2DZXYS in restoring passive learning and memory performance in AD rats is equivalent to donepezil hydrochloride. 3DZXYS increased SOD activity in the brain of model rats from 35.67±37.71 to (380.73±14.85)u/mg pr (P < 0.05). 4DZXYS reduced the MDA content in the brain of model rats from 7.88±0.70 to (6.64±0.80) ng/mg pr (P < 0.01). Conclusion : Reducing free radical damage is one of the main mechanisms of DZXYS to prevent AD model animal.