Erythropoietin inhibits the increase of intestinal labile zinc and the expression of inflammatory mediators after traumatic brain injury in rats.

BACKGROUND The objective of this study was to determine the effect of erythropoietin (Epo) on the intestinal labile zinc and the inflammatory factor in rats after traumatic brain injury (TBI). METHODS Male Sprague-Dawley rats were randomly divided into nine groups: (a) normal group; (b) sham-operation group; (c, d, e, f, and g) TBI group, killed at 1 hour, 6 hour, 24 hour, and 72 hour and 7 days postinjury, respectively; (h and i) TBI + saline and TBI + Epo, killed at 24 hour or 72 hour postinjury. Parietal brain contusion was produced by a free-falling weight on the exposed dura of the right parietal lobe. Intestinal labile zinc, the tumor necrosis factor-alpha, interleukin (IL)-8, and wet/dry weight ratio were investigated in different groups. RESULTS The gut contains a certain amount of labile zinc in normal animals and TBI caused obviously gradual increment of intestinal liabled zinc. The levels of inflammatory mediators and the gut wet/dry weight ratio were also found to increase in the trauma group (p < 0.05). There was a highly positive correlation between the abundance of zinc fluorescence and these proinflammation factors. Epo significantly reduced the intestinal labile zinc, the inflammatory mediators, and the gut wet/dry weight ratio compared with TBI group (p < 0.05). CONCLUSIONS Epo can protect intestine from TBI-induced injury by attenuating intestinal inflammation and labile zinc accumulation in vivo.