الفهرس 
Possible effects of certain natural products on thioacetamide-induced hepatotoxicity in rats
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Abstract
Protection against liver injury and its consequences is considered an essential issue to minimize the number of annual deaths caused by liver diseases. The present study was designed to evaluate the potential role of pomegranate peel extract (PPE) and/or curcumin, compared to silymarin in regression of thioacetamide (TAA)-induced liver injury, focusing on their modulatory effects on TGF-Ý/Smad3 and NF-mB signaling pathways. Hepatotoxicity was induced in adult male Wistar rats by intraperitoneal injection of TAA (100 mg/kg) three times a week, for 8 weeks. To assess the protective effects of PPE and/or curcumin against TAA-induced hepatotoxicity, compared to silymarin, rats were treated on a daily basis with oral doses of silymarin (50 mg/kg), curcumin (200 mg/kg), PPE (200 mg/kg), or a combination of PPE and curcumin, respectively for 8 weeks. The results indicated that treatment with silymarin, curcumin, PPE, or the combined therapy attenuated TAA-induced liver injury, as evidenced by significant improvement in the liver function tests (AST, ALT, ALP, total bilirubin, and albumin), oxidative stress biomarkers (MDA, SOD, and GSH), and inflammatory biomarkers (NF-{u0138}B, TNF-Ü, IL-1Ý, iNOS, TGF-Ý, and MPO), compared to TAA group. Moreover, administration of silymarin, curcumin, PPE, or the combined therapy exerted a significant downregulation of phospho-Smad3 protein expression; Ü-SMA, TIMP-1, and collagen-1 gene expressions, as well as significant reduction in liver Hyp content. The macroscopical, histopathological, and histochemical examinations have corroborated these findings. In conclusion, hepatoprotective activities of silymarin, curcumin, PPE, or the combined therapy could be linked to their abilities to modulate NF-mB, and TGF-Ý/Smad3 signaling pathways. It is worth noting that the combination of PPE and curcumin exerted superior hepatoprotective effects against TAA-induced liver injury, compared to monotherapy