一种白果清蛋白的抗衰老活性研究

目的研究白果清蛋白(GAP)对自然衰老小鼠及半乳糖致亚急性衰老模型小鼠的延缓衰老作用,并探讨作用机制。方法在半乳糖致亚急性衰老模型小鼠实验中,采用物理称重方法测定了GAP对小鼠脏器的影响,采用MTT法测定体外T、B淋巴细胞增殖作用,胸腺细胞增殖法测定GAP对细胞因子白细胞介素-2(IL-2)活性的影响,采用生化方法测定了血清中SOD的活性、GSH-Px的活性和MDA含量,采用机检法分析了GAP对小鼠血像的影响;在自然衰老小鼠实验中,分别进行了对小鼠免疫器官的影响实验、碳粒廓清作用实验、血清半数溶血值(HC50)实验以及二硝基氟苯诱导小鼠迟发型超敏反应(DTH)实验。结果GAP能增加半乳糖亚急性致衰老模型小鼠免疫器官的胸腺指数和脾脏指数,体外能促进活化和未活化的T、B淋巴细胞增殖及刺激脾淋巴细胞IL-2的分泌,能提高血液中白细胞的数量,增强小鼠的抗氧化能力;在自然衰老小鼠中,GAP能增加小鼠的胸腺指数和脾脏指数,增强自然衰老小鼠的巨噬细胞吞噬能力和DTH反应,促进血清溶血素的形成。结论GAP能在一定程度上延缓自然衰老小鼠及半乳糖亚急性致衰老模型小鼠的衰老过程,其作用机制可能与提高小鼠的免疫功能和抗氧化能力有关。

Studies on anti-aging activity of Ginkgo Albumin Protein(GAP )

Aim By using natural aging mice and D- galactose-induced subacute aging mice, Anti-aging effects of GAP were studied and the mechanism of the effects was discussed. Methods In the experiments of D-galactose-induced subacute aging mice, effect of GAP on viscera was determined by measuring body weight and organ weight. MTT method was employed to investigate T lymphocyte and B lymphocyte proliferation, thymocytes proliferation was employed to investigate activity of IL-2, SOD activity GSH-Px activity and MDA content in serum were determined using chemicalbiological methods, effect of GAP on hemogram in mice was analyzed by instrument analysis; In the experiments of natural aging mice, effect on immune organ, carbon granula clearance ability, serum hemolysin level, DTH induced by DNFB were determined. Results In the experiments of D-galactose-induced subacute aging mice, GAP showed good effects such as increasing thymus index and spleen index of model mice, promoting proliferation of activatied and inactivatied T, B lymphocyte in vitro, stimulating IL-2 secretion of lymphocyte, enhancing leucocyte number and antioxidative capacity of model mice. In the experiments of natural aging mice, GAP also showed good effects such as increasing spleen index and thymus index, enhancing phagocytosing ability of peritoneal macrophage and DTH reaction, promoting production of serum hemolysins immunized with SRBC. Conclusion GAP can delay aging process of D-galactose-induced subacute aging mice and natural aging mice in some degree, the mechanism maybe related to increasing immune function and antioxidative ability.