Betaine, a multifunction molecule, has a cardio protective feature but the mechanism is not well-understood. Hence, we evaluated the effect of betaine on cardiac tissue and serum biomarkers. Betaine administered to Albino rats at 50, 150 and 250 mg/kg, and sham group received deionized water. Myocardial infarction was induced by isoproterenol (100 mg/kg). The tunnel test and immunohistochemistry were performed on heart tissue to detect apoptosis and nitric oxide levels respectively. Serum levels of lipid peroxidation (LPO) and superoxide dismutase (SOD) were measured with colorimetric methods. The apoE and Bcl-2 gene expression were measured by RT-PCR in heart tissues and peripheral blood mononuclear cells (PBMCs). The results showed that betaine pretreatment at 250mg/kg for 60 days which reduces the apoptotic cells in the heart tissue after isoproterenol-induced myocardial infraction (P= 0.038). Cardiac Bcl-2 levels were upregulated by betaine, in which the maximum levels were observed in 150 mg/kg dosage. Similar finding was observed in the apoE expression in PBMCs. The tissue NOS levels were not change by betaine pretreatment significantly. Both superoxide dismutase and lipid peroxidation levels were reduced by betaine pretreatment dose dependently. Our results confirm the protective effect of betaine pretreatment that is mediated by Bcl-2 and anti-oxidative properties. تفاصيل المقالة

Tumor necrosis factor-α (TNFα) has several biological effects, including cell death, cell apoptosis and proliferation, and differentiation, as well as immune modulation. We characterized the alteration in TNF-α and the key receptors and molecular mediators related to TNF-α signaling pathway in the kidney after exposure to ethanol alone or in combination with curcumin (Cr). Accordingly, 24 male Wistar rats in 3 groups of control, ethanol, and Cr-treated - ethanolic groups were treated for six weeks. The ethanol group showed a significant elevation in TNF-α, nuclear factor-κB (NF-κB), and endothelin 1 (ET1) than the control group. TNF-α receptor 1 (TNFR1), TNF-α receptor 2 (TNFR2) and vascular endothelial growth factor receptor 2 (VEGFR2) were found with a significant down-regulation, and of TNF-receptor-associated factor 2 (TRAF2) and receptor-interacting protein-1 (RIP-1), and activator protein-1 (AP-1) were found with an up-regulation in the ethanol group than the control group. Cr and ethanol decreased the gene expression of TRAF-2, RIP-1 and AP-1, as well as increased the gene expression of TNFR1. Cr administration restored the increased levels of TNF-α, NF-κB and endothelin to these levels in the control group. Therefore, ethanol-related kidney injury addressed by our previous studies and others may in part be associated with the TNF-α signaling pathway, and such impacts can be rescued by Cr as an antioxidant and anti-inflammatory compound. تفاصيل المقالة