BMC ophthalmology · 2024
Protective effect of apelin-13 in lens epithelial cells via inhibiting oxidative stress-induced apoptosis.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Li Xue, Gu Chao, Hu Qiumei, Wang Liqin, Zhang Ya, Yu Ling
Аннотация
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, H2O2, apelin-13 + H2O2, ML221 + H2O2, and apelin-13 + ML221 + H2O2. ML221 was employed in rescue experiments as an APJ antagonist. HLECs were pretreated with or without apelin-13 and subsequently exposed to H2O2. 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 H2O2-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 H2O2-induced inhibition of the pentose phosphate pathway and dysregulation of cell redox status in the apelin-13 + H2O2 group compared with the H2O2 group. In H2O2-treated HLECs, apelin-13 can mitigate cell apoptosis, promote Bcl-2 expression, and suppress the Bax and Caspase-3 expression. In addition, H2O2 substantially reduced the mitochondrial membrane potential in HLECs, which was reversed by apelin-13. Notably, the inhibition of APJ intensified oxidative damage in H2O2-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.
METHODS: This experiment included five groups: control, H2O2, apelin-13 + H2O2, ML221 + H2O2, and apelin-13 + ML221 + H2O2. ML221 was employed in rescue experiments as an APJ antagonist. HLECs were pretreated with or without apelin-13 and subsequently exposed to H2O2. 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 H2O2-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 H2O2-induced inhibition of the pentose phosphate pathway and dysregulation of cell redox status in the apelin-13 + H2O2 group compared with the H2O2 group. In H2O2-treated HLECs, apelin-13 can mitigate cell apoptosis, promote Bcl-2 expression, and suppress the Bax and Caspase-3 expression. In addition, H2O2 substantially reduced the mitochondrial membrane potential in HLECs, which was reversed by apelin-13. Notably, the inhibition of APJ intensified oxidative damage in H2O2-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.