RESUMEN
BACKGROUND/AIMS: The effect of kefir on peptic ulcer disease was evaluated in an experimental model, with non-steroid anti-inflammatory drugs, together with the determination of gastric mucus secretion by quantitative digital histochemistry. MATERIALS AND METHODS: The experimental group included 28 male albino Wistar rats. After a diet with standard rat bait for 7 days, 14 rats were fed with kefir for 7 days while the others were kept on the same diet. At the 14th day, indomethacin was injected to 7 of the rats fed on kefir and to 7 of the rats on standard rat bait. All the rats were sacrificed after 4 hours. Gastric erosion and ulceration were scored histopathologically. Mucosal mucus was quantified by image analysis, and periodic acid-Schiff stained area percentage was determined. RESULTS: Erosion and ulceration were identified only in cases that received indomethacin. In the cases on kefir, erosion was identified in 6 cases (86%) and ulceration in 1 case. Rats fed on standard diet had erosion in 4 cases (57%) and ulceration in 3 (43%), but the difference was statistically insignificant (Mann-Whitney test, p=0.25). The stained area percentage for gastric mucus was not different between the four groups (Kruskal-Wallis test, p=0.313). CONCLUSIONS: These findings suggest that kefir does not change gastric mucus secretion. Although statistically insignificant, as there were more cases with ulceration in cases on the rat diet, kefir might have a beneficial effect on peptic ulcer disease induced by non-steroid anti-inflammatory drug. This requires further evaluation in larger series.
Asunto(s)
Productos Lácteos Cultivados , Mucosa Gástrica/patología , Úlcera Gástrica/patología , Úlcera Gástrica/prevención & control , Animales , Mucosa Gástrica/metabolismo , Indometacina , Masculino , Moco/metabolismo , Ratas , Ratas Wistar , Estadísticas no Paramétricas , Úlcera Gástrica/inducido químicamente , Úlcera Gástrica/metabolismoRESUMEN
BACKGROUND: Recent studies have suggested that EPO activates the CREB transcription pathway and increases BDNF expression and production, which contributes to EPO-mediated neuroprotection. We investigated whether EPO has a neuroprotective effect against ISCI in rats and examined the involvement of CREB protein phosphorylation in this process. METHODS: Spinal cord ischemia was produced by balloon occlusion of the abdominal aorta below the branching point of the left subclavian artery for 5 minutes, and rHu-EPO (1000 U/kg BW) was administered intravenously after the onset of the reperfusion. Neurologic status was assessed at 1, 24, and, 48 hours. After the end of 48 hours, spinal cords were harvested for histopathologic analysis and immunohistochemistry for pCREB. RESULTS: All sham-operated rats had a normal neurologic outcome, whereas all ischemic rats suffered severe neurologic deficits after ISCI. Erythropoietin treatment was found to accelerate recovery of motor deficits and prevent the loss of motoneurons in the spinal cord after transient ischemia. Ischemic spinal cord injury induced the phosphorylation of pCREB at the anterior horn of the spinal cord, and EPO treatment significantly potentiated expression of pCREB increase at the anterior horn of the spinal cord. CONCLUSIONS: These results demonstrate that a single dose of EPO given before ISCI provides significant neuroprotection and potentiates the expression of pCREB in this region.