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Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Drug+Chem+Toxicol 2017 ; 40 (1): 47-56 Nephropedia Template TP
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Comparative study of antifibrotic activity of some magnesium-containing supplements on experimental liver toxicity Molecular study #MMPMID27151930
El-Tantawy WH; Sabry D; Abd Al Haleem EN
Drug Chem Toxicol 2017[Jan]; 40 (1): 47-56 PMID27151930show ga
INTRODUCTION: Liver fibrosis is the excessive accumulation of extracellular matrix (ECM) proteins including collagen that occurs in most types of chronic liver diseases. This study aimed to investigate and compare the therapeutic efficacy of different magnesium (Mg)-containing supplements (formulations A, B, and C) on carbon tetrachloride (CCl(4))-induced liver fibrosis in rats. METHODS: Liver fibrosis was induced by intraperitoneal injection of rats with CCl(4) (1:1 in olive oil, 2 mL/kg, three times/week) for 4 weeks, and then rats were orally treated with different Mg-containing supplements (formulations A, B, and C) once daily for another one month. Liver fibrosis was quantified by evaluation of expressions of Collagen I, transforming growth factor beta-1 (TGFbeta1), platelet-derived growth factor-C (PDGF-C), nuclear factor kappa-beta (NF-kappabeta), and measurement of hepatic collagen (hydroxyproline) level. Also, malondialdehyde (MDA), nitric oxide (NO), glutathione (GSH) level, superoxide dismutase (SOD), and glutathione-S-transferase (GST) activities were estimated. RESULTS: CCl(4) administration significantly elevated expressions of the studied genes, hepatic hydroxyproline, MDA, and NO levels and caused depletion of GSH level, decreased SOD, and GST activities when compared with those of their corresponding control, p < 0.05. All magnesium supplements significantly inhibited expressions of the studied genes and attenuated the hepatic hydroxyproline level as compared with those of CCl(4)-treated group(;) p < 0.05; for NF-kappabeta, the highest inhibition was by formulations B and C. Regarding Collagen I, TGFbeta1, and hepatic hydroxyproline content, the highest inhibition was by Formulation C, and Formulation A revealed highest inhibition for PDGF-C. All magnesium supplements revealed normalization of oxidant and antioxidants parameters. Histopathological examination supports the biochemical and molecular findings. CONCLUSION: Mg supplements were effective in the treatment of hepatic CCl(4)-induced fibrosis-rat model.