Protective Role of L-Carnitine and Tocopherol Against Cold Restraint Stress Induced Gastric Lesions In Streptozotocin–Diabetic Rats

Abstract

In the present study, the influence of cold restraint stress (CRS)-induced gastric damage in diabetic rats, in relation to the antioxidative system was investigated. Male albino rats were used in the study, they were divided into 5 groups: i): non stressed group, ii): control CRS group, iii) diabetic CRS group (the rats of this group were injected with streptozotocin (STZ) 70 mg/kg i.p. and used 4 weeks after induction of diabetes with blood glucose levels of >350 mg/dl), iv): STZ L-carnitine pretreatment group (STZ-induced diabetic rat of this group were given L-carnitine 500 mg/kg 30 min before CRS) and v): STZ-vitamine E pretreatment group (STZ-induced diabetic rat of this group were given vitamin E 60 mg/kg body wt three weeks before CRS). The last four groups were exposed to CRS, at the end of each experiment, gastric damage was observed macroscopically. CRS induced gastric lesion, that was markedly exacerbated in STZ diabetic rats, but this aggravation was significantly suppressed by pretreatment with either L-carnitine or tocopherol (vitamin E) pretreatments. Diabetic rat stomachs showed significantly less glutathione peroxidase (GPX) activity as well as reduced glutathione (GSH) content than normal rat stomachs. In addition, the deleterious influence of diabetes on the gastric ulcerogenic response to CRS was significantly mitigated by decreasing lipid peroxidation by pretreatment with either L-carnitine or vitamin E. These results suggest that the gastric mucosa of diabetic rats is more vulnerable to cold restraint-induced injury, and the mechanism may be partly accounted for by impairment of the antioxidative system associated with a reduced GPX activity and GSH content. Based on these data, the beneficial effects of L-carnitine and vitamin E on CRS-induced mucosal injury especially in diabetics may be attributed to their antioxidative effects.