目的 研究八子補(bǔ)腎膠囊（BZBS）對快速衰老小鼠視網(wǎng)膜的保護(hù)作用。方法 將快速衰老小鼠SAMP6隨機(jī)分為模型組和BZBS（2.8 g·kg^-1）組，取抗快速老化SAMR1小鼠作為同源對照（對照組），每天ig給藥1次，對照組與模型組ig 0.9%氯化鈉溶液，連續(xù)給藥9周。HE染色觀察視網(wǎng)膜組織病理變化；試劑盒法檢測各組小鼠視網(wǎng)膜組織總抗氧化能力（T-AOC）、超氧化物歧化酶（SOD）、丙二醛（MDA）水平；Western blotting法檢測各組小鼠視網(wǎng)膜組織中衰老蛋白P21、P16和自噬蛋白P62、LC3 II/I表達(dá)水平。結(jié)果 與對照組相比，模型組小鼠視網(wǎng)膜外節(jié)段呈現(xiàn)空泡樣改變，內(nèi)外核層細(xì)胞數(shù)量減少且排列不連續(xù)，中間的叢狀層變?。籘-AOC、SOD水平顯著下降，MDA水平顯著上升（P<0.001）；衰老蛋白P16、P21表達(dá)顯著上調(diào)（P<0.001），自噬蛋白P62、LC3 II/I表達(dá)顯著下調(diào)（P<0.001）。與模型組比較，BZBS組小鼠視網(wǎng)膜病理改變得到明顯緩解；T-AOC、SOD水平均顯著上升，MDA水平顯著下降（P<0.05、0.01）；衰老蛋白P16、P21表達(dá)顯著下調(diào)（P<0.001），自噬蛋白P62、LC3 II/I表達(dá)均顯著上調(diào)（P<0.05、0.01）。結(jié)論 BZBS對快速衰老小鼠視網(wǎng)膜有保護(hù)作用，能夠減少視網(wǎng)膜病理改變，降低衰老蛋白表達(dá)，提高視網(wǎng)膜抗氧化水平；其作用機(jī)制可能與激活p62-LC3 II/I從而增強(qiáng)自噬有關(guān)。

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.

R285.5

天津市教委科研計(jì)劃項(xiàng)目（2021KJ137）