补肝散对衰老大鼠学习记忆能力及氧化损伤的影响

Effects of Bugan Powder on learning and memory ability and oxidative damage in aged rats

目的:观察补肝散对衰老大鼠学习记忆及氧化损伤的影响,探讨肝气虚损与衰老的关系。方法:将24只SPF级雄性SD大鼠随机分为空白对照组、模型组、补肝散组(14.06g·kg^(-1)·d^(-1))、吡拉西坦组(0.4g·kg^(-1)·d^(-1))。除空白对照组腹腔注射0.9%氯化钠溶液(10mL·kg^(-1)·d^(-1))外,其余3组腹腔注射D-半乳糖(400mg·kg^(-1)·d^(-1))诱导衰老大鼠模型。造模同时分别按照相应剂量给予药物干预,连续治疗8周。观察大鼠一般生物学特征;采用八臂迷宫和跳台实验评价大鼠学习记忆行为;测定脑、胸腺、脾脏、肝脏脏器指数及血清超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量。结果:与空白对照组比较,模型组大鼠记忆错误次数显著增多(P<0.01),跳台潜伏期显著缩短(P<0.01);脑、胸腺、脾脏、肝脏脏器指数显著下降(P<0.01,P<0.05);SOD活性显著降低(P<0.01),MDA含量显著升高(P<0.01)。与模型组比较,补肝散组大鼠记忆错误次数显著减少(P<0.05,P<0.01),跳台潜伏期显著延长(P<0.01);脑、胸腺、脾脏、肝脏脏器指数显著升高(P<0.01,P<0.05);SOD活性显著升高(P<0.01),MDA含量显著下降(P<0.05)。结论:补肝散可通过改善D-半乳糖致衰老大鼠氧化损伤程度从而提高学习记忆能力,此为探讨肝虚致衰理论提供了实验依据。

Objective: To observe the effects of Bugan Powder on learning and memory ability and oxidative damage in aging rats, and explore the relationship between liver-qi deficiency and aging. Methods: Twenty-four male SD rats with SPF grade were randomly divided into 4 groups: the control group, the model group, the Bugan Powder group(14.06 g · kg^(-1)·d^(-1)), and the Piracetam group(0.4 g · kg^(-1)·d^(-1)). Except for the control group, which was injected intraperitoneally with 0.9% sodium chloride solution(10 mL · kg^(-1)·d^(-1)), the other three groups were intraperitoneally injected with D-galactose(400 mg · kg^(-1)·d^(-1)) to induce the aging rat model. Meanwhile, each group was given drug intervention according to the corresponding dose, and the treatment lasted for 8 weeks. Observe the general biological characteristics of rats;evaluate the learning and memory behavior of rats with eight arm radical maze and step-down test;measure brain, thymus, spleen, liver organ index, serum superoxide dismutase(SOD) activity, and malondialdehyde(MDA) content. Results: Compared with the control group, in the model group, the number of memory errors was significantly increased(P<0.01), the step down latency was significantly shortened(P<0.01);the organ indexes of brain, thymus, spleen, and liver were remarkably decreased(P<0.01, P<0.05);the SOD activity was decreased(P<0.01), the MDA content was increased(P<0.01). Compared with the model group, in the Bugan Powder group, the number of memory errors was significantly reduced(P<0.05, P<0.01), the step down latency was significantly prolonged(P<0.01);the organ indexes of brain, thymus, spleen, and liver were increased(P<0.01, P<0.05);the SOD activity was increased(P<0.01), the MDA content was decreased(P<0.05). Conclusion: Bugan Powder can improve the ability of learning and memory by improving the degree of oxidative damage in D-galactose-induced aging rats, which provides an experimental basis for exploring the theory of aging induced by liver-qi deficiency.