目的 研究八子补肾胶囊（BZBS）对快速衰老小鼠视网膜的保护作用。方法 将快速衰老小鼠SAMP6随机分为模型组和BZBS（2.8 g·kg-1）组，取抗快速老化SAMR1小鼠作为同源对照（对照组），每天ig给药1次，对照组与模型组ig 0.9%氯化钠溶液，连续给药9周。HE染色观察视网膜组织病理变化；试剂盒法检测各组小鼠视网膜组织总抗氧化能力（T-AOC）、超氧化物歧化酶（SOD）、丙二醛（MDA）水平；Western blotting法检测各组小鼠视网膜组织中衰老蛋白P21、P16和自噬蛋白P62、LC3 II/I表达水平。结果 与对照组相比，模型组小鼠视网膜外节段呈现空泡样改变，内外核层细胞数量减少且排列不连续，中间的丛状层变薄；T-AOC、SOD水平显著下降，MDA水平显著上升（P<0.001）；衰老蛋白P16、P21表达显著上调（P<0.001），自噬蛋白P62、LC3 II/I表达显著下调（P<0.001）。与模型组比较，BZBS组小鼠视网膜病理改变得到明显缓解；T-AOC、SOD水平均显著上升，MDA水平显著下降（P<0.05、0.01）；衰老蛋白P16、P21表达显著下调（P<0.001），自噬蛋白P62、LC3 II/I表达均显著上调（P<0.05、0.01）。结论 BZBS对快速衰老小鼠视网膜有保护作用，能够减少视网膜病理改变，降低衰老蛋白表达，提高视网膜抗氧化水平；其作用机制可能与激活p62-LC3 II/I从而增强自噬有关。
Objective To study on the protective effect of Bazi Bushen Capsule (BZBS) on the retina of rapidly aging mice. Methods The rapidly aging SAMP6 mice were randomly divided into model group and BZBS (2.8 g·kg-1) group. The anti-rapidly aging SAMR1 mice were selected as homologous control group (control group). Mice in the model group and control group were given 0.9% sodium chloride solution, ig once a day for nine consecutive weeks. The total antioxidant capacity (T-AOC), the level of superoxide dismutase (SOD) and malondialdehyde (MDA) in the retina of mice in each group were tested by reagent kit method. HE staining was used to observe the pathological changes of retina. The expression of aging protein P21, P16 and autophagy protein P62, LC3 II/I in the retina of mice in each group were detected by Western blotting. Results Compared with control group, the outer segment of the retina in model group showed vacuolar changes, the number of cells in the inner and outer nuclear layers was reduced and the arrangement was discontinuous, and the middle plexiform layer was thinner. The content of T-AOC (P< 0.001) and SOD (P< 0.01) decreased significantly, while the content of MDA increased significantly (P< 0.001). The expression of aging proteins P16 (P< 0.001) and P21 (P< 0.001) was upregulated, while the expression of autophagy proteins P62 and LC3 II/I was downregulated (P< 0.001). After treatment with BZBS, the pathological changes in the retina of mice were alleviated, and the levels of T-AOC (P< 0.05) and SOD (P< 0.01) were significantly increased, while the content of MDA was significantly decreased (P< 0.01). The expression of aging proteins P16 (P< 0.001) and P21 (P< 0.001) was down regulated, while the expression of autophagy proteins P62 (P< 0.001) and LC3 II/I (P< 0.05) were up regulated. Conclusion BZBS has protective effect on the retina of agerelated macular degeneration model mice, can reduce the pathological changes of retina, reduce the expression of aging protein, and improve the antioxidant level of retina. Its mechanism may be related to the activation of p62-LC3 II/I to enhance autophagy.