The Histopathologic Effects of L-Carnitine in a Sodium Taurocholate-Induced Severe Pancreatitis Model

Abstract

This study aims to evaluate the histopathologic effects of L-carnitine (LC) in an experimental severe pancreatitis (SP) model induced with sodium taurocholate. LC is an amino acid-like molecule that plays an active role in transporting fatty acids and producing acetyl CoA in mitochondrial matrix for beta-oxidation to provide energy that is needed for metabolism. It has ameliorative effects on cell injury, as has been demonstrated in many studies. The present study focuses on evaluating the histopathologic effects of LC in an experimental SP model. A total of 32 Sprague-Dawley male rats were divided into 4 groups in a randomized fashion: control (C) group, L-carnitine (LC) group, pancreatitis (P) group, and pancreatitis and L-carnitine (P + LC) group. Pancreatitis was induced by a retrograde pancreatic duct injection of 4% sodium taurocholate, and LC was administered 200 mg/kg/d in the treatment group. Rats were euthanized with cardiac puncture under anesthesia at the 48th hour of the experiment for biochemical and histopathologic examination. In the P + LC group, the histopathologic findings of the pancreatitis were markedly reduced. Acinar cell degeneration was rarely seen. Interlobular and intralobular inflammation and edema was generally mild. The pancreatic damage score of the P + LC group was significantly lower than that of the P group (P < 0.05). This study revealed that LC has a significant histopathologic protective effect on acinar cell degeneration in a sodium taurocholate-induced SP model in rats.