衰老标记蛋白30（SMP30）是一种随年龄增加而减少的钙调节蛋白。本课题组前期证实SMP30在人晶状体上皮细胞（LECs）中有表达并与白内障密切相关，且与体外培养的人LECs系SRA01/04衰老相关，并具有抗氧化、抗凋亡及增加细胞活性等作用。有文献报道SMP30基因敲除鼠更易患白内障，但深入研究报道较少。据此提出假说：SMP30在动物模型水平上对LECs具有多重保护作用，其含量改变可能影响年龄相关性白内障（ARC）的发生发展。为验证假说，本实验拟探索Wistar大鼠LECs中SMP30的表达与年龄的关系；同时在Wistar大鼠即将发生/发生ARC时，眼内注射携带SMP30高表达/沉默基因的腺病毒载体进行干预，观察晶状体结构及LECs相关指标的变化，探索与SMP30作用密切相关的蛋白和基因，研究SMP30对LECs的保护作用及预防和治疗ARC的效果，为ARC的防治提供新的研究方向。

Senescence marker protein 30 (SMP30) is a calcium-regulated protein that decreases with ages. Our previous researches have confirmed that SMP30, which is expressed in human lens epithelial cells (LECs), is closely related to cataract formation and the senescence of LECs line SRA01/04 cultured in vitro. Meanwhile, SMP30 plays a part in promoting anti-oxidative, anti-apoptotic and cell proliferation activities in SRA01/04. It has been reported that SMP30 knockout mice is more susceptible to cataract, but in-depth studies on SMP30 animal models are still rare. Therefore, a hypothesis is proposed: SMP30 has multiple protective effects on LECs at the animal models, and the changes of SMP30 content may affect the occurrence and development of age-related cataract (ARC). To verify the hypothesis, further research will be carry out: 1）exploring the relations between age and the expression of SMP30 in Wistar rat’s LECs; 2) When ARC is about to occur/develop, intraocular injection of adeno-associated virus vector encoding SMP30 over-expression/knockdown gene is used for interventional therapy. Next, we will observe the changes of lens structure and LECs related indicators, and explore the proteins and genes related to SMP30. This experiment aims to study the effect of SMP30 on LECs and ARC, so as to provide a new research direction for the prevention and treatment of ARC.