羊毛甾醇是胆固醇合成通路中的重要中间产物，具有抗氧化作用与逆转晶状体蛋白凝聚功能。而紫外线是白内障发病的重要环境因素，那么它是否通过影响羊毛甾醇含量与功能促使老年性白内障的发生？最近，我们发现实际到达晶状体内紫外线强度数十倍低于目前国际眼晶状体细胞实验紫外线暴露水平，且UVB小于UVA近30倍。因此，本研究拟以UVA照射试管内附着羊毛甾醇的脂质体和晶状体蛋白凝聚体，探讨紫外线对羊毛甾醇逆转晶状体蛋白凝聚功能的影响。通过照射晶状体上皮细胞，探讨照射产生的氧化型羊毛甾醇和氧化型胆固醇对乙酰辅酶A还原酶的负性调节作用；探讨照射产生的表观遗传修饰对羊毛甾醇合酶表达的抑制，以期阐明UVA对眼晶状体羊毛甾醇及其上游主要限速酶负性调节机制，并加以慢性动物实验验证。为紫外线致白内障发病机制提供新的依据。

Lanosterol is an important intermediate in cholesterol biosynthesis pathway, which has the functions of antioxidation and reversal of lens protein aggregation. While UV is an important environmental factor in the pathogenesis of cataract, it remains unclear if UV contributes to cataract formation by inhibiting the function and content of lanosterol . Recently, we have found that the UV intensity actually reaching lens was ten folds lower than the current international UV exposure level in lens cell experiments, and UVB exposure intensity is nearly 30 times less than that of UVA.In this project, liposome constructed and attached with lanosterol will be irradiated with UVA in vitro, being mixed with lens protein. Then, the lens epithelial cells will be treated with UVA. We will quantify the effect of ultraviolet radiation on the lanosterol function of reversal lens proteins aggregation, characterize the negative regulative role of oxidized lanosterol and oxysterols to acetyl coenzyme A reductase, and describe the epigenetic effect of UV on the expression inhibition of lanosterol synthase. We will clarify the negative regulative mechanism of UVA on the ocular lens lanosterol and its upstream main rate limiting enzyme, and validate our findings in chronic animal experiments. The results may provide the experimental basis for the pathogenesis of cataract induced by ultraviolet radiation and bring preventive and therapeutic benefits.