Planta Med 2022; 88(15): 1471
DOI: 10.1055/s-0042-1759091
Poster Session I

Asiatic acid inhibits pro-oxidant mediators-induced oxidative stress in human aortic endothelial cells

LY Fong∗
1   Department of Preclinical Sciences, Faculty of Medicine and Health Sciences, Universiti Tunku Abdul Rahman, Kajang, Malaysia
,
N N Mohd Razali
1   Department of Preclinical Sciences, Faculty of Medicine and Health Sciences, Universiti Tunku Abdul Rahman, Kajang, Malaysia
,
C T Ng
2   Unit of Physiology, Faculty of Medicine, AIMST University, Bedong, Malaysia
,
Y K Yong
3   Department of Human Anatomy, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, Malaysia
,
M N Hakim
4   Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, Malaysia
,
Y M Lim
1   Department of Preclinical Sciences, Faculty of Medicine and Health Sciences, Universiti Tunku Abdul Rahman, Kajang, Malaysia
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Oxidative stress, characterized by an imbalance between the synthesis of pro-oxidant molecules and antioxidant mechanisms in cells, is a hallmark of early atherosclerosis. Hence, inhibition of oxidative stress could be a promising approach in prevention of atherosclerosis and the associated cardiovascular diseases. Asiatic acid is a major terpenoid isolated from Centella asiatica L. Urban and exhibits pharmacological activities including anti-hypertensive, cardioprotective and anti-hyperlipidemic activities [1]. However, the knowledge gap on how asiatic acid acts on oxidative stress that occurs in the endothelium remains unaddressed. The objective of this study was to assess the effect of asiatic acid on tumor necrosis factor alpha (TNF-α)- or hydrogen peroxide (H2O2)-stimulated oxidative stress using human aortic endothelial cells. Intracellular reactive oxygen species (ROS) levels and the activity of catalase (CAT) were evaluated. The protein expression of p47phox, which is a subunit of NADPH oxidases (No X) that generates ROS, was also assessed using Western blot analysis. The results showed that 40 µM of asiatic acid inhibited TNF-α-induced increased ROS release. Asiatic acid, at 10 – 40 µM, was found to prevent reduced CAT activity elicited by H2O2. Our optimization data also demonstrated that 10 ng/mL of TNF-α upregulated p47phox expression maximally at 1 h. Yet, asiatic acid did not suppress the increased p47phox expression. These findings indicate that asiatic acid alleviates endothelial oxidative stress by decreasing ROS production and enhancing CAT activity. But the exact Nox subunit which attributes to antioxidant effect of asiatic acid warrants further investigations. The authors declared no conflict of interest.

Funding

This work was funded under Fundamental Research Grant Scheme (FRGS/1/2018/SKK06/UTAR/02/7) by the Ministry of Higher Education, Malaysia


 


Publication History

Article published online:
12 December 2022

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