الفهرس 
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Abstract
Sodium diclofenate is one of nonsteroidal anti-inflammatory drugs that has fatal hepato-nephrotoxicity side effects. While allicin is the most vital organosulfer compound with health enhancing properties. This study was designed to evaluate the protective effects of allicin against sodium diclofenate-induced hepato-nephrotoxicity in rats. Sixty adult male wister albino rats were randomly divided into six groups. First group received calcium carbonate and corn starch at a dose of 0.75 mg/kg BW orally for 30 days. Second group received sodium diclofenate at a dose of 2 mg/kg BW orally for 30 days. Third group received allicin at a dose of 45 mg/kg BW orally for 30 days. Fourth group administrated sodium diclofenate as the second group and allicin at a dose of 15 mg/kg BW orally simultaneously for 30 days. Fifth group received sodium diclofenate as the second group and allicin at a dose of 30 mg/kg BW orally simultaneously for 30 days. Sixth group received
sodium diclofenate and allicin as second and third groups, respectively for 30 days.
Sodium diclofenate-induced hepato-nephrotoxicity represented by significant elevation of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities and levels of creatinine and urea. In addition, it induced hyperglycemia, hepatic lipid peroxidation, pathological alteration and expression of caspase-3 protein in hepatic and renal tissues and proliferating cell nuclear antigen protein (PCNA) in hepatic tissue. However, it decreased antioxidant biomarker, Glutathione (GSH) concentration. In contrast, allicin modulated the sodium diclofenate-induced alterations in hepatic and renal functions and structures in a dose dependent manner.
This study indicated that allicin has a potential protective effects against sodium diclofenate-induced hepato-nephrotoxicity in rats.