Camel Milk Attenuates Cardiotoxicity Induced by Monosodium Glutamate via Inhibition of Oxidative Stress and Inflammation in Rats

Abstract

Monosodium glutamate (MSG), a widely used food additive, has been implicated in cardiotoxic effects through mechanisms involving oxidative stress, inflammation, and apoptosis. Camel milk (CM), known for its antioxidant and anti-inflammatory properties, may offer protective effects against such toxicity. This study evaluated the cardioprotective potential of CM against MSG-induced cardiac damage in rats. Forty male Wistar rats (185-205 g) were randomized into four groups (n = 10): Control (distilled water), MSG (6 g/kg), MSG + CM (MSG 6 g/kg + CM 5 ml/kg), and Recovery (MSG 6 g/kg followed by 21 days without CM treatment). All treatments were administered orally for 21 days. Body and heart weights were recorded. Cardiac tissues were assayed for myeloperoxidase (MPO), nitric oxide (NO), C-reactive protein (CRP), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), NF-κB, malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH), glutathione-S-transferase (GST), glutathione peroxidase (GPx), caspase-3 activity, and DNA fragmentation index. Histopathological evaluation of the myocardium was performed. Data were analyzed by one-way ANOVA with Tukey's post hoc test (p < 0.05). MSG significantly increased inflammatory (MPO, NO, CRP, IL-1β, TNF-α, NF-κB), oxidative (MDA), apoptotic (caspase-3), and DNA damage markers, while reducing antioxidant enzyme activities (CAT, SOD, GSH, GST, GPx) and heart weight (p < 0.05). CM restored antioxidant defenses, lowered inflammatory and apoptotic indices, reduced DNA fragmentation, and preserved myocardial architecture. The recovery group exhibited partial but less pronounced improvements. Camel milk effectively mitigates MSG-induced cardiotoxicity, highlighting its importance as a natural cardioprotective dietary intervention.