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Preclinical trial of avocado pulp supplementation in an L-NAME model of cardiovascular injury

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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. Methods Male rats were randomized into six groups (n = 4 per group): control, avocado, L-NAME, L-NAME+drugs (metoprolol+losartan), L-NAME+avocado, and L-NAME+drugs+avocado. Morphometric indices, lipid profiles, cardiac injury enzymes, and vascular biomarkers were measured after treatment. One-way ANOVA with Tukey test assessed group differences, while contour plots and correlation networks visualized biomarker interactions. Results L-NAME treatment 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 reprogramming pathological biomarker networks toward control-like organization Highlights Avocado supplementation improves lipid balance, cardiac integrity, and vascular function in L-NAME–induced injury. Contour and network analyses reveal avocado disrupts maladaptive biomarker couplings and restores control-like organization. Preclinical evidence supports avocado as a nutraceutical adjunct for integrated cardiometabolic protection. GRAPHICAL ABSTRACT
Title: Preclinical trial of avocado pulp supplementation in an L-NAME model of cardiovascular injury
Description:
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.
Methods Male rats were randomized into six groups (n = 4 per group): control, avocado, L-NAME, L-NAME+drugs (metoprolol+losartan), L-NAME+avocado, and L-NAME+drugs+avocado.
Morphometric indices, lipid profiles, cardiac injury enzymes, and vascular biomarkers were measured after treatment.
One-way ANOVA with Tukey test assessed group differences, while contour plots and correlation networks visualized biomarker interactions.
Results L-NAME treatment 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 reprogramming pathological biomarker networks toward control-like organization Highlights Avocado supplementation improves lipid balance, cardiac integrity, and vascular function in L-NAME–induced injury.
Contour and network analyses reveal avocado disrupts maladaptive biomarker couplings and restores control-like organization.
Preclinical evidence supports avocado as a nutraceutical adjunct for integrated cardiometabolic protection.
GRAPHICAL ABSTRACT.

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