Amadi, P. | bioRxiv Science

bioRxiv2025

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

BackgroundEndothelial 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. MethodsMale 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. ResultsL-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. ConclusionAvocado 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 HighlightsO_LIAvocado supplementation improves lipid balance, cardiac integrity, and vascular function in L-NAME-induced injury. C_LIO_LIContour and network analyses reveal avocado disrupts maladaptive biomarker couplings and restores control-like organization. C_LIO_LIPreclinical evidence supports avocado as a nutraceutical adjunct for integrated cardiometabolic protection. C_LI GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=152 SRC="FIGDIR/small/681762v1_ufig1.gif" ALT="Figure 1"> View larger version (36K): org.highwire.dtl.DTLVardef@12bc02borg.highwire.dtl.DTLVardef@1558740org.highwire.dtl.DTLVardef@229d49org.highwire.dtl.DTLVardef@843627_HPS_FORMAT_FIGEXP M_FIG C_FIG

pharmacology and toxicology↗

bioRxiv2025

Avocado supplementation mitigates hypertension and multi-organ injury in an L-NAME model of cardiovascular dysfunction

BackgroundEndothelial dysfunction, hypertension, and multi-organ injury remain central drivers of cardiovascular disease. Avocado (Persea americana) is rich in monounsaturated fatty acids, phytosterols, and antioxidants, yet its integrative impact on hypertension-induced systemic injury has not been fully explored. MethodsMale Wistar rats (n = 4/group) were randomized into six groups: control, avocado, L-NAME, L-NAME+losartan+metaprolol succinate, L-NAME+avocado, and L-NAME+metaprolol succinate+avocado. Avocado pulp was incorporated into diet at 80% w/w. Endpoints included blood pressure indices, hematological parameters, liver enzymes, renal function tests, and correlation analyses of systolic-diastolic coupling. One-way ANOVA with Tukeys post hoc tests evaluated group differences, while forest plots and scatter analyses visualized treatment effects. ResultsL-NAME significantly elevated systolic blood pressure ({Delta}+18 mmHg), diastolic pressure ({Delta}+20 mmHg), and mean arterial pressure ({Delta}+17 mmHg; all p < 0.01) compared with controls. Avocado supplementation reduced these elevations by ~15-18 mmHg, restoring values near baseline. L-NAME increased platelet counts (p = 0.031) and trended toward leukocytosis, both of which were attenuated by avocado. ALT levels were higher in L-NAME rats (p = 0.044), while AST and ALP trended upward; avocado-fed groups maintained near-control enzyme levels. Renal markers were most affected: urea (+25 mg/dl) and creatinine (+0.8 mg/dl) rose significantly in L-NAME rats (p < 0.01), but were reduced by 20-30% with avocado supplementation. Electrolytes remained unchanged. Correlation analyses revealed pathological SBP-DBP coupling in L-NAME rats (r = 0.78), abolished by avocado (r = 0.00). ConclusionAvocado supplementation mitigates L-NAME-induced hypertension and systemic injury by stabilizing blood pressure, reducing thrombocytosis, and preserving hepatic and renal function. These findings support avocado as a pleiotropic nutraceutical adjunct for cardiometabolic protection. HighlightsO_LIAvocado pulp supplementation incorporated into chow (80% w/w) mitigates L-NAME-induced hypertension in rats. C_LIO_LIDietary avocado preserves hepatic and renal biochemical function while reducing thrombocytosis under cardiovascular stress. C_LIO_LIAvocado demonstrates pleiotropic nutraceutical potential, stabilizing systemic physiology beyond conventional pharmacological therapy. C_LI Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=106 SRC="FIGDIR/small/681766v1_ufig1.gif" ALT="Figure 1"> View larger version (31K): org.highwire.dtl.DTLVardef@101b300org.highwire.dtl.DTLVardef@8f0624org.highwire.dtl.DTLVardef@1dc4ab3org.highwire.dtl.DTLVardef@1ac4130_HPS_FORMAT_FIGEXP M_FIG C_FIG

physiology↗