Investigation of Protective Effect of l-Carnitine on l-Asparaginase-Induced Acute Pancreatic Injury in Male Balb/c Mice

Introduction The present analysis deals with the biochemical and histopathological effects of l -carnitine in mice with l -asparaginase (ASNase)-induced experimental acute pancreatic injury (API). Methods A total of 32 male Balb/c mice were divided into four groups as follows. Group I (control) was...

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Veröffentlicht in:Digestive diseases and sciences 2015-05, Vol.60 (5), p.1290-1296
Hauptverfasser: Kaya, Inan, Citil, Mehmet, Sozmen, Mahmut, Karapehlivan, Mahmut, Cigsar, Gulsen
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Sprache:eng
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Zusammenfassung:Introduction The present analysis deals with the biochemical and histopathological effects of l -carnitine in mice with l -asparaginase (ASNase)-induced experimental acute pancreatic injury (API). Methods A total of 32 male Balb/c mice were divided into four groups as follows. Group I (control) was injected with single saline via the intraperitoneal route. Group II received 500 mg/kg of l -carnitine daily with the injected volume of 62.5–75 μl for 25–30 g mice using a Hamilton microinjector applied for 5 days. Group III received a single 10,000 IU Escherichia coli ASNase/kg body weight dose of ASNase at a dose of 500 mg/kg. Group IV received 500 mg/kg of l -carnitine daily and a single dose of 500 mg/kg of ASNase and were decapitated on the fifth day following the injection. Blood and pancreatic tissue samples were obtained for evaluation of histopathological structure and levels of malondialdehyde (MDA), reduced glutathione (GSH), total sialic acid (TSA), glucose, amylase and triglyceride. Results In group III, compared to group IV and group I it was determined that levels of GSH and amylase were significantly lower while levels of MDA, TSA, glucose and triglyceride were higher. Levels of GSH, MDA, TSA, glucose, triglyceride and amylase, especially in group IV, approached that of group I. As a result, l -carnitine for ASNase-induced API mice may be protective against pancreatic tissue degeneration and oxidative stress or lipid peroxidation.
ISSN:0163-2116
1573-2568
DOI:10.1007/s10620-014-3461-3