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Published:
Aug 7, 2026DOI:
10.4314/jdan.v17i1.1Keywords:
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Main Article Content
Preclinical trial of avocado pulp supplementation in an L-NAME model of cardiovascular injury
Abstract
Background: Endothelial dysfunction, dyslipidemia, and myocardial injury are major contributors to cardiovascular disease. Avocado (Persea americana), rich in monounsaturated fatty acids and phytochemicals, has shown lipid-lowering and anti-inflammatory properties, but its integrated effects on vascular injury remain unclear.
Objectives: The study evaluated the proof-of-concept evidence on the effect of avocado pulp supplementation on multi-system pathological phenotype (metabolic dysfunction, dyslipidemia, myocardial stress and vascular activation) in an L-NAME rat model of cardiovascular injury.
Methods: Male rats were randomized into six groups (n = 4 per group): control (normal chow, water only), avocado (normal chow + avocado + water only), L-NAME, L-NAME+drugs (metoprolol+losartan), L-NAME+avocado, and L-NAME+drugs+avocado (Groups 1 to 6, respectively). Morphometric indices, lipid profiles, cardiac injury enzymes, and vascular biomarkers were measured after treatment. One-way ANOVA with Tukey’s test assessed group differences, while contour plots and correlation networks visualized biomarker interactions.
Results: L-NAME treatment to groups 3 to 6 induced a pathological phenotype characterized by reduced feed efficiency (–40%), weight gain (–80%), and BMI (–18%), together with dyslipidemia (LDL +120%, TG +55%, TC +42%, HDL –28%), myocardial stress (troponin +70%, CK +50%, LDH +35%), and vascular activation (endothelin +350%, VCAM-1 +55%, AngII +80%; all p < 0.01). Avocado supplementation mitigated these effects: BMI and feed efficiency returned to near-control levels, LDL, TG, and TC fell by 30–45%, and troponin, CK, and LDH decreased by ~25–30%. Endothelin, VCAM-1, and AngII were reduced by 40–55% relative to L-NAME. Network analysis revealed dense pathological correlations under L-NAME (density 0.42), simplified under avocado (0.17), and most normalized with avocado+drugs (0.09), indicating restoration of physiological biomarker independence.
Conclusion: Avocado supplementation attenuates L-NAME–induced vascular injury by improving metabolic efficiency, correcting dyslipidemia, reducing cardiac injury, and dampening endothelial activation, while proposing a potential capacity to shift the pathological biomarker network towards a more control-like organization in such a preclinical proof-of-concept- study.
