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Methyl Palmitate, a Potent Angiotensin Converting Enzyme Inhibitor, Attenuates Vascular Remodeling in L-NG-Nitro Arginine Methyl Ester-Induced Hypertensive Wistar Rat Models
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DOI：10.1159/000551278.png)
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Abstract
En 中文
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 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 & micro;m, 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.
Keywords:
Angiotensin converting enzyme
Methyl palmitate
Blood pressure
ACE inhibition
Malondialdehyde
Nitric oxide
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J
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2.3
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