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目的观察改构型酸性成纤维细胞生长因子(maFGF)对D-半乳糖致衰老大鼠脑组织SOD活力、MDA含量和羟自由基含量及神经细胞凋亡的影响,探讨maFGF对慢性衰老大鼠的抗衰老作用。方法选择成年Wistar大鼠48只,采用皮下注射D-半乳糖建立衰老模型,衰老模型成功后随机分为衰老模型组、生理盐水(NS)对照组和maFGF治疗组。另16只不注射D-半乳糖作为正常对照组。各组大鼠到相对应的时间点取出脑组织,测定脑组织中SOD活力、MDA含量和抑制羟自由基能力;TUNEL法测定大鼠大脑皮质神经细胞凋亡数目。结果衰老模型组大鼠脑组织SOD活力显著降低,MDA含量和羟自由基含量升高,皮质神经细胞凋亡数明显增多;经过用maFGF治疗慢性衰老大鼠后脑组织SOD活力显著升高,MDA含量和羟自由基含量均显著降低,皮质神经细胞凋亡数明显减少。结论 maFGF起到降低自由基,提高脑组织的抗氧化能力,减少皮质神经细胞凋亡数量,具有抗衰老
Objective To investigate the effect of mafGF on the activity of SOD, the content of MDA and the content of hydroxyl radical and the apoptosis of neurons in the brain of aging rats induced by D-galactose, Anti-aging effect. Methods Forty-eight adult Wistar rats were selected and subcutaneously injected with D-galactose to establish the aging model. The aging model was randomly divided into aging model group, NS control group and maFGF treatment group. The other 16 rats were not injected D-galactose as a normal control group. The brain tissues of rats in each group were taken out at the corresponding time points, and the activity of SOD, the content of MDA and the inhibition of hydroxyl radical in brain tissue were measured. The number of apoptotic neurons in cerebral cortex was measured by TUNEL. Results The SOD activity in the brain tissue of aging model group was significantly lower, the contents of MDA and hydroxyl radical increased, and the number of apoptosis in cortical neurons increased significantly. After the treatment of chronic aging rats with maFGF, the SOD activity was significantly increased, and the MDA content And hydroxyl radical content were significantly decreased, the number of apoptotic cortical neurons decreased significantly. Conclusion maFGF can reduce free radicals, increase the antioxidant capacity of brain tissue, reduce the number of cortical neuronal apoptosis, have anti-aging