Home | About PM | Editorial board | Search | Ahead of print | Current Issue | Archives | Instructions | Subscribe | Advertise | Contact us |  Login 
Pharmacognosy Magazine
Search Article 
  
Advanced search 
 
ORIGINAL ARTICLE
Year : 2020  |  Volume : 16  |  Issue : 67  |  Page : 7-12

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


1 College of Traditional Chinese Medicine, Jinan University, Guangzhou; Nanhai Hospital of Traditional Chinese Medicine, Foshan, Guangdong, China
2 College of Traditional Chinese Medicine, Jinan University, Guangzhou, China

Correspondence Address:
Guoping Zhao
527 Room, College of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong 510630
China
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/pm.pm_631_18

Rights and Permissions

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.


[FULL TEXT] [PDF]*
Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)
 

 Article Access Statistics
    Viewed179    
    Printed7    
    Emailed0    
    PDF Downloaded67    
    Comments [Add]    

Recommend this journal