Department of Public Health and Preventive Medicine, Jinan University, Guangzhou 510632, China.
Department of Ophthalmology, the First Affiliated Hospital, Jinan University, Guangzhou 510632, China.
J Agric Food Chem. 2020 Aug 5;68(31):8286-8294. doi: 10.1021/acs.jafc.0c03194. Epub 2020 Jul 22.
Diabetic cataract is one of the most important causes of blindness worldwide. Cyanidin-3--glucoside (C3G) is found to exert beneficial effects on many diabetic complications. However, its effect on diabetic cataract is not well known. Herein, we investigated the effect of C3G on high glucose-induced lens epithelial cell (SRA01/04) apoptosis and cataract formation as well as the involved mechanisms. We found C3G (20 μM) could preserve cell viability in SRA01/04 cells exposed to high glucose (100 μM). Meanwhile, C3G inhibited SRA01/04 cell apoptosis and regulated the Bcl-2/Bax ratio. Additionally, C3G suppressed NF-κB activation and subsequent cyclooxygenases-2 (Cox-2) expression, which are associated with the protection against apoptosis. Moreover, C3G attenuated lens opacity and protein aggregation in lens culture exposed to high glucose. In conclusion, C3G protected against high glucose-induced SRA01/04 cell apoptosis and cataract formation, which indicated the potential protection of anthocyanins on diabetic cataract.
糖尿病性白内障是全球最重要的失明原因之一。矢车菊素-3-O-葡萄糖苷（C3G）被发现对许多糖尿病并发症有有益的影响。然而，其对糖尿病性白内障的作用尚不清楚。在此，我们研究了 C3G 对高糖诱导的晶状体上皮细胞（SRA01/04）凋亡和白内障形成的影响及其相关机制。我们发现 C3G（20 μM）可在暴露于高葡萄糖（100 μM）的 SRA01/04 细胞中保持细胞活力。同时，C3G 抑制 SRA01/04 细胞凋亡并调节 Bcl-2/Bax 比值。此外，C3G 抑制 NF-κB 激活及随后的环氧化酶-2（Cox-2）表达，这与对凋亡的保护有关。此外，C3G 减轻了高糖培养的晶状体中晶状体混浊和蛋白质聚集。总之，C3G 可防止高糖诱导的 SRA01/04 细胞凋亡和白内障形成，表明花色苷对糖尿病性白内障具有潜在的保护作用。
