Protective effect of apelin-13 in lens epithelial cells via inhibiting oxidative stress-induced apoptosis.

BACKGROUND

It is widely accepted that glaucoma-induced oxidative stress expedites cataracts' process. Therefore, we examined the effects of apelin-13 against oxidative stress-induced damage in human lens epithelial cells (HLECs) and investigated the potential pathogenic mechanism of acute primary angle-closure glaucoma.

METHODS

This experiment included five groups: control, HO, apelin-13 + HO, ML221 + HO, and apelin-13 + ML221 + HO. ML221 was employed in rescue experiments as an APJ antagonist. HLECs were pretreated with or without apelin-13 and subsequently exposed to HO. HLECs' viability was assessed by CCK8. Cell apoptosis was determined using Annexin V-FITC/PI staining. The mitochondrial membrane potential was assessed by fluorescent probe JC-1. Intracellular G6PD activity, NADPH/NADP+, and GSH/GSSG ratios were detected to assess the cells' oxidative damage.

RESULT

Apelin-13 reversed the HO-induced decrease in cell viability. The increased expression of G6PD and GLTU1, the G6PD, GSH/GSSG and NADPH/NADP + levels showed that apelin-13 can mitigate the HO-induced inhibition of the pentose phosphate pathway and dysregulation of cell redox status in the apelin-13 + HO group compared with the HO group. In HO-treated HLECs, apelin-13 can mitigate cell apoptosis, promote Bcl-2 expression, and suppress the Bax and Caspase-3 expression. In addition, HO substantially reduced the mitochondrial membrane potential in HLECs, which was reversed by apelin-13. Notably, the inhibition of APJ intensified oxidative damage in HO-induced HLECs, demonstrating that the effects of apelin-13 were hindered by ML221.

CONCLUTIONS

Apelin-13 reduced oxidative damage and apoptosis in HLECs through APJ. These results demonstrate that apelin-13 can be employed as a potential drug for glaucoma with cataracts to delay the progression of cataracts.