Resveratrol protects lens epithelial cells and delays cataract development via inhibiting TXNIP mediated oxidative stress and apoptosis.

BACKGROUND

As the predominant cause of blindness, cataract pathogenesis centrally involves oxidative stress-induced damage and apoptosis in lens epithelial cells. Although resveratrol possesses recognized antioxidant and antiapoptotic activities, its functional role in cataract development and its specific impact on TXNIP require further elucidation. This study aimed to investigate whether resveratrol delays cataract progression by regulating the TXNIP/Trx2 pathway, improving mitochondrial function, and inhibiting apoptosis.

METHODS

In vitro, an oxidative stress model was established using the hydrogen peroxide (H2O2)-induced human lens epithelial cell line B3 (HLE-B3), whereas in vivo, a cataract model was constructed in sodium selenite-induced SD rats. Evaluations included cell viability, ROS levels, mitochondrial function (mitoROS and ΔΨm), antioxidant markers (GSH, SOD, and CAT), expression of TXNIP, Trx2, and apoptosis-related proteins (cleaved-caspase-3, Bax, Bcl-2), and apoptosis detection. Lenticular opacity and histopathological changes were assessed in vivo.

RESULTS

In vitro experiments demonstrated that resveratrol and SRI37330 comparably suppressed H2O2-induced TXNIP expression and mitochondrial translocation, thereby upregulating Trx2, reducing ROS production, improving mitochondrial membrane potential, enhancing antioxidant capacity, and attenuating apoptosis. In vivo experiments revealed that resveratrol alleviated lens opacity and tissue abnormalities in rats, restored antioxidant function, regulated the expression of TXNIP, Trx2, and apoptosis-related proteins, and inhibited apoptosis.

CONCLUSION

Resveratrol delays cataract formation and progression by inhibiting TXNIP expression and mitochondrial translocation, restoring the mitochondrial antioxidant protein Trx2 expression, thereby reducing mitochondrial oxidative stress-related damage and blocking the mitochondrial apoptotic pathway.