补阳还五汤对阿尔茨海默病小鼠海马凋亡因子及学习记忆能力的影响

目的:探讨补阳还五汤(BYHWT)对阿尔茨海默病小鼠海马组织凋亡因子及学习记忆能力的影响。方法:40只雄性APP/PS1双转基因小鼠随机分为模型组,多奈哌齐组(0.001 g·kg~(-1)),BYHWT高、中、低剂量组(分别为37.06,18.53,9.26 g·kg~(-1))。C57小鼠作为空白组。连续灌胃BYHWT 30 d,进行水迷宫行为学测试后,取材。用蛋白免疫印迹法(Western blot)检测小鼠海马中凋亡因子B细胞淋巴瘤/白血病-2(Bcl-2),Bcl-2相关X蛋白(Bax)和半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)的变化。结果:与空白组比较,模型组小鼠学习记忆能力明显降低,海马组织中凋亡因子Bcl-2明显减少(P0.01),Bax和Caspase-3明显增加(P0.01)。与模型组比较,BYHWT高、中剂量组能明显改善小鼠学习记忆能力,凋亡因子Bcl-2明显增加(P0.01),Bax和Caspase-3明显减少(P0.01)。结论:补阳还五汤能够明显改善阿尔茨海默病小鼠的学习记忆能力,降低海马组织中Bax和Caspase-3的表达,增加Bcl-2的表达。

Effect of Buyang Huanwutang on Hippocampal Apoptosis Factors and Learning and Memory Abilities in Mice with Alzheimer's Disease

Objective:To observe the effect of Buyang Huanwutang (BYHWT) on the apoptosis factors in hippocampus and learning and memory abilities of Alzheimer''s disease mice. Method:Totally 40 male APP/PS1 double transgenic mice were randomly divided into 5 groups:model group, donepezil group (0.001 g·kg^-1), high-dose, middle-dose and low-dose BYHWT groups (with the dosage of 37.06, 18.53, 9.26 g·kg^-1, representatively). Another 8 C57 mice were used as control group. After 30 days of administration, Morris water maze behavior test was conducted; and after the test, all mice were put to death. Western blot was used to detect the changes in apoptotic factors in hippocampus of the mice:B-cell lymphoma-2 (Bcl-2), Bcl-2 associated X protein (Bax) and cysteine aspartate protease-3 (Caspase-3). Result:Compared with the control group, the learning and memory abilities of the model group were significantly lower (P<0.01), Bcl-2 in hippocampus was obviously reduced (P<0.01), and Bax and Caspase-3 increased significantly (P<0.01). Compared with the model group, high-dose and middle-dose BYHWT groups could significantly improve the learning and memory abilities of the mice, Bcl-2 increased significantly (P<0.01), and Bax and Caspase-3 decreased significantly (P<0.01). Conclusion:BYHWT can obviously improve the learning and memory abilities of Alzheimer''s disease mice, reduce the expressions of Bax and Caspase-3 in hippocampus, and increase the expression of Bcl-2.