Protective effect of ferulic acid on human umbilical vein endothelial cell model of cold stress

Protective effect of ferulic acid on human umbilical vein endothelial cell model of cold stress

Context: Ferulic acid (FA) is an active principle derived from the traditional Chinese medicine Angelica sinensis, which has been used for the treatment of cardiovascular and cerebrovascular diseases in China for many years. However, a thorough understanding of effects on vascular function by FA has not been investigated. 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.

背景：阿魏酸（FA）是一种源自中药当归的活性成分，在中国多年来一直用于治疗心脑血管疾病。然而，FA对血管功能影响的全面了解尚未得到研究。 目的：本研究的目的是通过抑制瞬时受体电位阳离子通道M亚家族成员8（TRPM8）通道以及调节内皮型一氧化氮（NO）通路来改善人脐静脉血管内皮细胞（HUVECs）的寒冷暴露损伤，从而探究FA的潜在机制。 研究对象和方法：采用3 -（4,5 - 二甲基噻唑 - 2 - 基）- 2,5 - 二苯基四氮唑溴盐测定法和乳酸脱氢酶（LDH）测定法检测寒冷暴露和FA对细胞活力的影响。利用定量聚合酶链反应和蛋白质印迹法检测HUVECs中TRPM8、缺氧诱导因子 -α（HIF - 1α）、内皮素 - 1（ET - 1）、诱导型一氧化氮合酶（iNOS）、内皮型一氧化氮合酶（eNOS）的信使RNA和蛋白质表达。采用酶联免疫吸附测定法检测HUVECs培养上清液中ET - 1的浓度。 结果：18°C的寒冷暴露对细胞形态无显著影响，但增加了LDH和ET - 1的分泌以及TRPM8、HIF - 1α、iNOS和ET - 1的表达。FA处理降低了所有这些变化。寒冷应激模型中NO和eNOS水平降低，而FA处理减轻了寒冷诱导的NO和eNOS的降低。 结论：寒冷应激可导致如TRPM8和ET - 1等血管收缩剂增加并降低细胞活力，但FA可通过调节细胞中这些物质的表达来预防寒冷应激相关的心脑血管疾病。