Abstract
Cataract is a disease that causes severe visual impairment in patients. Recent studies have found that lens epithelial cell apoptosis caused by oxidative damage is the critical cause of cataract. Moreover, TRIM22 could alleviate the ubiquitination of TRAF6. The expression of TRAF6 could activate the p38/MAPK pathway and aggravate the oxidative stress induced damage of lens epithelial cells. However, whether the TRIM22 could alleviate the oxidative stress induced damage of lens epithelial cells by regulating the expression of TRAF6 and p38/MAPK pathway is unclear. In this study, we stimulated the lens epithelial cells with the H2O2 and established the TRIM22 knockdown cells. Next, proliferation of these cells was determined by CCK-8 and EdU assays. Apoptosis of these cells was detected with the TUNEL assays. Levels of ROS was explored with the DCFH-DA staining. Finally, the expression levels of TRAF6, p-p38 and p-ERK were determined with the western blotting. According to the results, we found that knockdown of TRIM22 suppressed the proliferation and relieved the H2O2 induced DNA double-strand break and apoptosis of these cells. Inhibition of TRIM22 inhibited the production of ROS in these cells. Moreover, restriction of TRIM22 induced the decreased levels of TRAF6, p-p38 and p-ERK in lens epithelial cells. We concluded that inhibition of TRIM22 relieved the apoptosis of lens epithelial cells by suppressing the expression of TRAF6, p-p38 and p-ERK.