Preliminary study on the effect of trauma-induced secondary cellular hypoxia in brain injury

Secondary cerebral hypoxia has recently been shown to play an important role in the outcome of patients suffering from traumatic brain injury (TBI). However, the precise mechanisms underlying secondary cerebral hypoxia are complex and interrelated. In this study, we investigate the effect of hypoxia within a rat model of trauma-induced late cerebral cortex injury. Using the hypoxia marker pimonidazole, we verified and isolated areas of the cortex that had suffered hypoxic damage. Using subsequent reverse-transcriptase PCR analyses, we found that the expressions of both transforming growth factor β1 (TGF-β1) and hypoxia-inducible factor-1α (HIF-1α) increased significantly under hypoxic conditions induced by TBI compared with uninjured control animals. In addition, the maximum mRNA expression of TGF-β1 and HIF-1α was found at 3 days and 12 h after TBI, respectively. Our data suggest that secondary cerebral hypoxia injury involves various cytokines including TGF-β1 and HIF-1α. Furthermore, upon immunohistochemical analysis, both TGF-β1 and HIF-1α expression were almost localized in the same types of cells by using immunohistochemical study. These results may have important implications in the understanding of trauma-induced secondary cerebral hypoxia injury.