Protective effect of L-carnitine against ethanol-induced gastric damage: investigation of possible mechanisms of action

Authors : Emrah İPEK, Şule Yurdagül ÖZSOY

Pages : 73-83

Doi:10.31797/vetbio.1264050

View : 91 | Download : 62

Publication Date : 2023-08-30

Article Type : Research Paper

Abstract :The underlying mechanisms of L-carnitine’s insert ignore into journalissuearticles values(L-CAR); protective effect against ethanol insert ignore into journalissuearticles values(EtOH);-induced gastric mucosal damage were investigated in this study. The rats were randomly divided into four groups: control insert ignore into journalissuearticles values(CON);, EtOH, EtOH + L-CAR50, and EtOH + LCAR100. Control group was given saline insert ignore into journalissuearticles values(5 mL/kg); twice at 1-hour interval. EtOH group was given 5 mL/kg saline 1-hour before absolute EtOH administration insert ignore into journalissuearticles values(5 mL/kg);. EtOH + LCAR50 group received 50 mg/kg LCAR 1-hour before absolute EtOH administration insert ignore into journalissuearticles values(5 mL/kg);. EtOH + LCAR100 group received 100 mg/kg LCAR 1-hour before absolute EtOH administration insert ignore into journalissuearticles values(5 mL/kg);. All the rats were euthanized 1 hour after the administration of EtOH. The gastric lesion area was grossly examined, and gastric lesions were histopathologically evaluated. Real-time PCR was used to examine the expression of cyclooxygenase 1 and 2 insert ignore into journalissuearticles values(COX-1 and COX-2);, inducible- and endothelial- nitric oxide synthase insert ignore into journalissuearticles values(iNOS and eNOS);, tumor necrosis factor alpha insert ignore into journalissuearticles values(TNF-α);, heat shock protein 70 insert ignore into journalissuearticles values(HSP70);, and trefoil factor 2 insert ignore into journalissuearticles values(TFF2); mRNA in the gastric mucosa. Histopathological examination revealed that L-CAR treatment reduced the severity and extent of gastric lesions caused by EtOH administration, such as shedding of the superficial epithelium, glandular gland necrosis, intralesional hemorrhage, submucosal edema, and neutrophil infiltration. L-CAR administration was found to significantly reduce the mRNA levels of COX-2, iNOS, eNOS, and TNF-α in the gastric mucosa compared to EtOH administration alone. It was determined that L-CAR administration further increased the gastric mucosal HSP70 mRNA expression than EtOH administration alone. L-CAR treatment increased TFF2 expression which was decreased after EtOH administration. Finally, L-CAR administration was thought to protect against EtOH-induced gastric mucosal damage by regulating the expression of gastric mucosal COX and NOS systems, reducing the inflammatory cytokine levels, inducing a cellular stress response, and stimulating the expression of factors associated with mucus secretion and gastric epithelium restitution.
Keywords : cyclooxygenase, ethanol, heat shock protein, L carnitine, nitric oxide synthetase, trefoil peptides