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Excessive food additives Monosodium glutamate (MSG) results in metabolic disorders with increased Cardiovascular diseases CVD. We aimed to emphasise berberine (BBR) effect on MSG induced metabolic syndrome (MetS) and its associated endothelial dysfunction. Newborn rats were divided into control group, MSG group (4 mg/g) each other day for the first 14 days of life and MSG + BBR group that was given MSG then BBR in dose 150 mg/kg/day for 6 weeks. Body weight, food intake, systolic blood pressure, biochemical metabolic and oxidative stress markers were evaluated. Aortic tissue homogenate Endothelin −1 (ET-1) and matrix metalloproteinase −1 (MMP-1) assessment, in addition to histological and EM examination were done. Newborn rats MSG exposure results in typical adult life MetS and oxidative stress with significant increase in ET-1 and MMP-1with aortic vasculopathy. BBR significantly improved all the disturbed parameters; suppress increased body weight (BW), food intake (FI) and partly improved the aortic vasculopathy lesions, holding a promise for BBR as a defending agent against MSG metabolic and vascular disorders.HIGH LIGHT MSGMSG is frequently consumed as a flavour enhancer especially between children and adolescentExcessive utilisation MSG is associated MS with vascular endothelial dysfunctionMMP-1 may be involved in atherosclerotic plaque formationBBR has beneficial outcome for metabolic disorders induced by MSG among newly born ratsBBR has a role in management vascular inflammation and remodelling MSG is frequently consumed as a flavour enhancer especially between children and adolescent Excessive utilisation MSG is associated MS with vascular endothelial dysfunction MMP-1 may be involved in atherosclerotic plaque formation BBR has beneficial outcome for metabolic disorders induced by MSG among newly born rats BBR has a role in management vascular inflammation and remodelling

archives of physiology and biochemistry

Berberine alleviates monosodium glutamate induced postnatal metabolic disorders associated vascular endothelial dysfunction in newborn rats: possible role of matrix metalloproteinase-1