EFFECT OF G-CSF ON ETHANOL-INDUCED HEMORRHAGIC GASTRITIS MODEL IN DIABETES MELLITUS-INDUCED RATS

Abstract

Diabetes mellitus can affect every organ system, including large and small vessels, eyes, nerves, kidneys and gastrointestinal system. Acid peptic disease is an inflammatory condition involving the upper gastrointestinal tract. The elevated serum glucose levels of diabetics affect traditional host defenses such as neutrophil counts and functions. We aimed to investigate changes of gastric mucosa and the role of impaired neutrophil functions in a diabetes-induced experimental model and whether G-CSF, which modulates neutrophil counts and function, has protective effects against gastric mucosal injury in diabetic rats.

Fifty rats were divided into three groups. Diabetes mellitus was induced by a single dose of streptozotocin in 40 of 50 rats. Controls had a sham injection. The gastric mucosal lesions were produced by intragastric administration of 1 ml of 95% ethanol in all three groups. Granulocyte colony-stimulating factor (G-CSF) was subcutaneously injected to twenty of diabetes-induced rats. Stomach histology and tissue malondialdehyde and glutathione levels were determined. White blood cell count, neutrophil counts and functions were determined.

Peripheral blood cell counts, neutrophil phagocytosis index were decreased but neutrophil adhesivity index was not different in diabetes-induced groups. G-CSF administration improved neutrophil counts and function. Macroscopic and microscopic gastric mucosal injury were significantly greater in control and only diabetes group compared with G-CSF pretreated group (p < 0.05). The tissue malondialdehyde and glutathione levels were significantly decreased in G-CSF-administrated diabetic group compared to untreated diabetics (p < 0.001).

Finally, G-CSF has been shown to cause neutrophilia and improve neutrophil phagocytosis in diabetic. G-CSF may be cytoprotective for gastric mucosa in diabetes mellitus-induced rats.