Protective Effect of Ferulic Acid on Human Umbilical Vein Endothelial Cell Model of Cold Stress

Aims: The aim of the present study was to investigate the potential mechanism of FA by suppressing Transient receptor potential cation channel subfamily M member 8 (TRPM8) channels and regulating endothelial nitric oxide (NO) pathway to ameliorate cold explore injury in human umbilical vascular endothelial cells (HUVECs). Subjects and Methods: The effects of cold exposure and FA on cell viability were detected by 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide assay and lactate dehydrogenase (LDH) assay. Quantitative polymerase chain reaction and Western blot were utilized to detect TRPM8, hypoxia‑inducible factor‑alpha (HIF‑1α), endothelin‑1 (ET‑1), inducible NO synthase (iNOS), endothelial NO synthase (eNOS) messenger RNA, and protein expression in HUVECs. Enzyme‑linked immunosorbent assay method was used to detect the concentration of ET‑1 in culture supernatants of HUVECs. Results: Cold exposure at 18°C had no significant effect on cell morphology but increased secretion of LDH and ET‑1 and the expression of TRPM8, HIF‑1α, iNOS, and ET‑1. Treatment with FA decreased all of these changes. The levels of NO and eNOS decreased in cold stress model, while FA treatment attenuated the cold‑induced decrease of NO and eNOS. Conclusion: Cold stress can cause an increase in vasoconstrictors such as TRPM8 and ET‑1 and reducing cell viability, but FA can prevent cold stress‑related cardiovascular disease by regulating the expression of these substances in cells.