Saudi Journal of Gastroenterology
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ORIGINAL ARTICLE
Year : 2009  |  Volume : 15  |  Issue : 3  |  Page : 156-162

Protective effect of L-arginine against necrosis and apoptosis induced by experimental ischemic and reperfusion in rat liver


1 Cellular and Microbiology Laboratory, College of Pharmacy, IFTM, Lodhipur Rajput, Moradabad - 244 001, UP and Pharmacy Group, Birla Institute of Technology and Sciences, Pilani - 333 031, Rajasthan, India
2 National Biotechnology Center, Indian Veterinary Research Institute. Izatnagar - 243 312, UP, India
3 Cellular and Microbiology Laboratory, College of Pharmacy, IFTM, Lodhipur Rajput, Moradabad - 244 001, UP, India

Correspondence Address:
Pronobesh Chattopadhyay
Microbiology and Cell Biology Laboratory, College of Pharmacy, IFTM, Lodhipur Rajput, Moradabad-244 001, UP
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1319-3767.45356

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Background/Aim: To study the effect of L-arginine on apoptosis and necrosis induced by 1-h ischemia followed by 3-h reperfusion. Materials and Methods: Adult Wistar rats underwent 60 min of partial liver ischemia followed by 3-h reperfusion. Eighteen Wistar rats were divided into sham-operated control group (I) ( n = 6), ischemia and reperfusion (I/R) group (0.9 % saline (5 mL/kg, orally) for 7 days) (II) ( n = 6), and L-arginine-treated group (10 mg/kg body weight daily orally for 7 days before inducing ischemia-reperfusion maneuver) (III) ( n = 6). Apoptotic and necrotic hepatocytes, nitric oxide levels in hepatocytes, Bcl-2 mRNA, and Bcl-2 protein were measured. Liver injury was assessed by plasma alanine transaminases (ALT), aspartate transaminases (AST), liver histopathology, and electron microscopy. Results: An ischemic and reperfusion hepatocellular injury occurred as was indicated by increased serum ALT, AST, histopathology, and electron microscopy. Apoptosis and necrosis associated marker gene Bcl-2 mRNA and protein expression were decreased in I/R group. Pretreatment with L-arginine significantly decreased serum ALT and AST level and apoptotic and necrotic cells after 1 h ischemia followed by 3 h of reperfusion. Nitric oxide production in hepatocytes was increased twofold by L-arginine treatment when compared with I/R group. Histopathology and transmission electron microscopy (TEM) studies showed markedly diminished hepatocellular injury in L-arginine-pretreated rats during the hepatic I/R. Conclusion: Thus, it may be concluded that L-arginine afforded significant protection from necrosis and apoptosis in I/R injury by upregulated Bcl-2 gene and nitric oxide production.


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