Supplementary Material for: Methyl Palmitate, a potent Angiotensin Converting Enzyme inhibitor attenuates vascular remodelling in L-NG-Nitro Arginine Methyl Ester-induced hypertensive Wistar rat models

Introduction:Angiotensin Converting Enzyme (ACE) regulates blood pressure via the renin-angiotensin and bradykinin systems.Though synthetic ACE inhibitors are more effective, they pose several side effects.Methyl Palmitate (MP), a natural fatty acid methyl ester with cytoprotective, antioxidant, anti-inflammatory, and vasodilatory properties, is not explored for its ACE inhibitory or antihypertensive potential.This study aimed to investigate the in vitro ACE inhibition of MP and its effect on L-NG-Nitro Arginine Methyl Ester (L-NAME)-induced hypertensive male Wistar rats. Methods:An in vitro ACE inhibition assay was conducted to compare the ACE inhibition potency of MP with that of Lisinopril.Male Wistar rats (n = 35, 7 per group) were grouped into control, disease control, and treatment groups receiving 100, 150, or 200 mg/kg/day of MP for 21 days each.Blood pressure, serum ACE activity, malondialdehyde (MDA), and nitric oxide (NO) levels in kidney tissue homogenate, and thoracic aorta histopathology were assessed. Results:MP inhibited ACE by 61.05% at 5 µM, exceeding Lisinopril’s 41.67%. High-dose MP significantly reduced serum ACE and MDA levels, while increasing NO (p < 0.001).Histopathology revealed near-normal vasculature, although changes in blood pressure were not statistically significant (p > 0.05).Conclusion:MP demonstrates strong natural ACE inhibition, antioxidant, and vascular protective effects, supporting further research for therapeutic optimization.