【摘要】 本研究旨在探讨EGCG的抗衰老作用及对小鼠脑组织NF-κB蛋白表达的影响。首先通过颈背部皮下注射D-半乳糖诱导建立小鼠衰老模型,并对衰老程度进行鉴定;其次,利用EGCG处理衰老小鼠,以超氧化物歧化酶(SOD)活性和β-半乳糖苷酶活性确定EGCG的抗衰老作用;最后,进一步利用蛋白免疫印迹方法检测EGCG对脑组织衰老相关信号分子NF-κB-P65和IκBα(Y42)蛋白表达的影响。研究结果表明:成功建立了小鼠衰老模型,并发现小鼠衰老后出现记忆能力下降等行为学变化;外周血SOD活性下降;脑组织IκBα表达下调,NF-κB蛋白表达被激活。而EGCG处理后,血清SOD活性恢复,IκBα表达呈上调趋势,NF-κB蛋白表达被抑制。因此,本研究发现EGCG具有明显抗衰老作用,其机制可能通过抑制NF-κB的表达而阻碍了细胞衰老的进程。该研究结果为EGCG相关的抗衰老保健品开发提供了一个新的方向。更多还原

【Abstract】 Epigallocatechin-3-gallate( EGCG) from green tea extract has natural antioxidant activity,and its correlation with the animal aging process remains unclear. In this study,d-galactose-induced senescent mouse models were firstly established. EGCG treatment at a dosage of 1 mg /( kg·d) was performed for 5 weeks. Memory ability of mice,SOD activity in serum,and senescence-associated β-galactosidase activity at hippocampus neurons were detected to estimate aging process. Furthermore,the gene expressions of NF-κB and IκB-α in brain tissue were analyzed through Western blotting after EGCG treatment. As a result,the d-galactose-induced senescent mouse models were successfully established with lower memory ability. SOD activity in serum was decreased and NF-κB expression in brain tissue was up-regulated for senescent mouse. After EGCG treatment for senescent mice,SOD activity in serum was recovered,and expression of NF-κB was inhibited,while IκB-α expression had a up-regulated tendency. Our results demonstrated that EGCG can block the aging process,and the mechanism was possibly related to the inhibition of NF-κB expression. These results can provide a novel direction for studying on the function of EGCG against aging.更多还原