Cardiorenal Protective Effects of Allicin Derived from Allium sativum Against High-Salt Diet-Induced Hypertension in Sprague-Dawley Rats

Abstract

Background: Cardiovascular diseases (CVDs) remain a leading cause of illness and death worldwide, and phytochemicals from medicinal plants have attracted growing attention as cardioprotective agents. This study investigated the cardio-renal protective effects of allicin, an organosulfur compound derived from Allium sativum (garlic), against hypertension and associated organ damage induced by a high-salt diet (HSD) in Sprague-Dawley (SD) rats.

Methods: Hypertension was induced in rats with L-NAME (16 mg/kg, i.p.) followed by an 8% high-salt diet. Allicin (16 mg/kg, i.p.) was administered for 21 days, with amlodipine (1 mg/kg) included as a positive control. Serum lipid profile, liver enzymes (ALT, AST), haematological indices, urinary electrolytes and diuretic activity, cardiac and renal histopathology, and the expression of IL-6, TNF-α, NOX, caspase-3, VCAM-1 and ET-1 were evaluated. Molecular docking was additionally performed to assess the binding of allicin to eNOS, IL-6 and TNF-α.

Results: HSD administration raised cholesterol, triglycerides and LDL, elevated ALT and AST, disturbed haematological parameters (haemoglobin, haematocrit, platelet count, RBC), and caused tubular dilation in the kidney and haemorrhage in the myocardium, alongside increased expression of IL-6, TNF-α, NOX, caspase-3, VCAM-1 and ET-1. Twenty-one days of allicin treatment reversed these biochemical and histopathological changes and lowered the inflammatory markers. Allicin also significantly increased urine output and urinary sodium excretion, indicating diuretic and natriuretic activity, while potassium loss was only mildly attenuated, suggesting a potassium-sparing effect. Molecular docking identified eNOS, IL-6 and TNF-α as plausible binding targets for allicin.

Conclusion: Allicin protects against HSD-induced cardiac and renal injury by reversing lipid, hepatic, haematological and histopathological abnormalities, suppressing inflammatory signalling, and preserving electrolyte balance. These findings support allicin as a promising candidate for further development as an adjunct therapy for hypertension-associated organ damage.