Tectorigenin significantly attenuated radiation-induced oxidative stress and apoptosis in human umbilical vein endothelial cells by suppressing the activation of PINK1-mediated mitophagy.
Does Tectorigenin prevent irradiation-induced injury in HUVECs?
Tectorigenin protects endothelial cells from radiation-induced injury by inhibiting PINK1/Parkin-mediated mitophagy, offering a potential candidate for preventing radiation-induced heart disease.
p-value: p=<0.05
OBJECTIVE: This study aimed to investigate the protective effect of Tectorigenin against irradiation-induced endothelial cell damage and to elucidate the underlying mechanism, thereby identifying potential therapeutic targets for irradiation-induced heart disease. METHODS: radiation-induced injury model was established to evaluate oxidative stress and apoptosis. Mitochondrial morphology was assessed by transmission electron microscopy, while mitochondrial function was evaluated using JC-1 staining, MitoSOX staining, immunofluorescence, and ATP assays. To investigate the involvement of mitophagy in the underlying mechanism, a mitophagy inhibitor, PINK1 siRNA, and PINK1 overexpression were employed. RESULTS: Tectorigenin significantly attenuated radiation-induced oxidative stress and apoptosis, suppressed mitochondrial reactive oxygen species (ROS) generation and membrane depolarization, and attenuated mitophagy activation through downregulation of PINK1 and Parkin expression. Notably, PINK1 inhibition potentiated these protective effects, whereas PINK1 overexpression abrogated Tec-mediated protection. CONCLUSION: Tectorigenin alleviated irradiation-induced injury through suppressing the activation of PINK1-mediated mitophagy, thereby offering potential therapeutic targets and candidate agents for radiation-induced heart disease (RIHD).
Liu et al. (Mon,) conducted a other in Irradiation-induced endothelial cell damage. Tectorigenin vs. Irradiation alone (9 Gy) was evaluated on Apoptosis and oxidative stress (p=<0.05). Tectorigenin significantly attenuated radiation-induced oxidative stress and apoptosis in human umbilical vein endothelial cells by suppressing the activation of PINK1-mediated mitophagy.