Fig. 5: GPR39 knockout mitigates Ang II-induced endothelial cell injury.
From: Targeting GPR39 in structure-based drug discovery reduces Ang II-induced hypertension
a–e Evaluation of apoptosis-related protein levels (P-eNOS, eNOS, Bax, Bcl-2, Caspase-3 and Cleaved caspase-3, n = 6) in HUVECs across PBS, Ang II, si-GPR39, and Ang II + si-GPR39 groups. GAPDH was employed as the loading control. f TUNEL staining to visualize apoptosis in the four HUVEC groups (TUNEL, green; DAPI, blue; n = 6; Scale, 50 μm). White arrows highlight endothelial cells with elevated TUNEL expression. g Cellular activity in the four groups was assessed using a CCK8 kit, reflecting enzymatic activity (n = 6). h ROS staining to detect oxidative stress in HUVECs of the four groups (ROS, green; DAPI, blue; n = 6; Scale, 50 μm). White arrows highlight endothelial cells with elevated ROS expression. i–l Quantitative analysis of mRNA levels of inflammatory markers (IL-1, IL-6, TNF-α and Nlrp3, n = 6) in HUVECs. Data are expressed as mean ± SEM. Statistical significance is denoted as NS (not significant), *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.
