Hypoxic Preconditioning Suppresses Glial Activation and Neuroinflammation in Neonatal Brain Insults

Figure 3

Hypoxia preconditioning reduces proinflammatory gene expression in neonatal hypoxia-ischemia brain injury. (a) The mRNA levels of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β) in the ipsilateral cerebral cortex from neonatal rats were determined at 2 and 6 h after hypoxia-ischemia (HI) injury ( in each group). The gene expression levels were upregulated by HI injury, especially at 6 h after injury. Hypoxia preconditioning (HP + HI) was able to significantly suppress these responses. (b) The protein concentrations of TNF-α and IL-1β were determined by ELISA at different time points ( in each group). The suppression of inflammatory mediators in the HP + HI group was significant at 6 h after HI. ((a), (b)) Data represented as the mean ± standard error of the mean (SEM). compared with HI, compared with HI, and for COX-2 mRNA level at 6 h for HP + HI group compared with HI group.

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