Abstract
BackgroundSonchus asper possesses antioxidant capacity and is used in liver and kidney disorders. We have investigated the preventive effect of methanolic extract of Sonchus asper (SAME) on the gentamicin induced alterations in biochemical and morphological parameters in liver and kidneys of Sprague-Dawley male rat.MethodsAcute oral toxicity studies were performed for selecting the therapeutic dose of SAME. 30 Sprague-Dawley male rats were equally divided into five groups with 06 animals in each. Group I received saline (0.5 ml/kg bw; 0.9% NaCl) while Group II administered with gentamicin 0.5 ml (100 mg/kg bw; i.p.) for ten days. Animals of Group III and Group IV received gentamicin and SAME 0.5 ml at a dose of 100 mg/kg bw and 200 mg/kg bw, respectively while Group V received only SAME at a dose of 200 mg/kg bw. Biochemical parameters including aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), γ-glutamyltransferase (γ-GT), total cholesterol, triglycerides, total protein, albumin, creatinine, blood urea nitrogen (BUN), total bilirubin and direct bilirubin were determined in serum collected from various groups. Urinary out puts were measured in each group and also assessed for the level of protein and glucose. Lipid peroxides (TBARS), glutathione (GSH), DNA injuries and activities of antioxidant enzymes; catalase (CAT), peroxidase (POD) and superoxide dismutase (SOD) were determined in liver and renal samples. Histopathological studies of liver and kidneys were also carried out.ResultsOn the basis of acute oral toxicity studies, 2000 mg/kg bw did not induce any toxicity in rats, 1/10th of the dose was selected for preventive treatment. Gentamicin increased the level of serum biomarkers; AST, ALT, ALP, LDH, γ-GT, total cholesterol, triglycerides, total protein, albumin, creatinine, BUN, total and direct bilirubin; as were the urinary level of protein, glucose, and urinary output. Lipid peroxidation (TBARS) and DNA injuries increased while GSH contents and activities of antioxidant enzymes; CAT, POD, SOD decreased with gentamicin in liver and kidney samples. SAME administration, dose dependently, prevented the alteration in biochemical parameters and were supported by low level of tubular and glomerular injuries induced with gentamicin.ConclusionThese results suggested the preventive role of SAME for gentamicin induced toxicity that could be attributed by phytochemicals having antioxidant and free radical scavenging properties.
Highlights
Sonchus asper possesses antioxidant capacity and is used in liver and kidney disorders
Effect of SAME on liver marker enzymes Gentamicin increased the level of biochemical parameters; aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and g-GT in serum as compared to that of the control group (Table 1)
Effect of SAME on serum biochemistry Injection of gentamicin to rats for ten days significantly (P < 0.01) decreased the serum level of total protein and albumin while the level of total cholesterol, triglycerides, total and direct bilirubin increased than that of the control group (Table 2). Altered level of these parameters induced with gentamicin in serum was restored, dose dependently, with the simultaneous treatment of SAME to rats than that of the control group
Summary
Sonchus asper possesses antioxidant capacity and is used in liver and kidney disorders. We have investigated the preventive effect of methanolic extract of Sonchus asper (SAME) on the gentamicin induced alterations in biochemical and morphological parameters in liver and kidneys of Sprague-Dawley male rat. The main problem associated with gentamicin is the cause of nephrotoxicity at its therapeutic doses and appeared to be a major cause of nonoliguric acute renal failure [1]. Gentamicin is Gentamicin causes the activation of platelet activation factor ensuing local vasoconstriction and reduces the renal blood flow and glomerular filtration rate [4]. Gentamicin induced renal injuries are mostly localized to the proximal tubules because of association of gentamicin with polyanionic inositol phospholipids and megalin, a receptor, for uptake of gentamicin [5,6]. Oxidative stress is mainly regulated by the cellular enzymatic (catalase, superoxide dismutase, glutathione peroxidase) and nonenzymatic (glutathione, ascorbic acid, a-tocopherol) factors [7]
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