Fig. 6: GPR39 knockdown mitigates Ang II-induced HUVEC injury by inhibiting Nlrp3.
From: Targeting GPR39 in structure-based drug discovery reduces Ang II-induced hypertension
a–e Analysis of protein levels (P-eNOS, eNOS, Bax, Bcl-2, Caspase-3 and Cleaved caspase-3, n = 6) in HUVECs across. 6 groups. GAPDH served as the loading control. f TUNEL staining to assess apoptosis in the 6 groups of HUVECs (TUNEL, green; DAPI, blue; n = 6; Scale, 50 μm). White arrows highlight endothelial cells with elevated TUNEL expression. g Evaluation of cellular activity in the PBS, Ang II, Ang II + si-GPR39, Nigericin, Nigericin + Ang II and Nigericin + Ang II + si-GPR39 groups using a CCK8 kit (n = 6). h ROS staining depicting oxidative stress in HUVECs of the 6 groups (ROS, green; DAPI, blue; n = 6; Scale, 50 μm). White arrows highlight endothelial cells with elevated ROS expression.0.1. i–l Measurement of mRNA levels of inflammation markers (IL-1, IL-6, TNF-α and Nlrp3, n = 6) in HUVECs. Results are expressed as the mean ± SEM, with statistical significance indicated as NS, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.
