Abstract
This study was performed to investigate the effects of prohormone thyroxine (T4) and the underlying mechanisms in the post‐ischemic rat brain after transient focal cerebral ischemia‐induced brain injury. Ischemic injury was induced for 2 h by middle cerebral artery occlusion (MCAO) followed by 24‐h reperfusion. T4 was administered by intra‐peritoneally injection twice, at 1 after the onset of ischemia and 6 h after reperfusion. The mechanism of neuroprotective effect of T4 was investigated with a focus on inflammatory cells, neurotrophins, and transcriptional factors. The results obtained showed that T4 significantly reduced cerebral infarction, which were accompanied by decreased expression of proapotptic Bax and increased antiapoaptotic Bcl‐2 protein. T4, also suppressed the activation of astrocytes and microglia, increased the expression of neurotrophic factors (BDNF, GDNF), and suppressed up‐regulation of inflammatory‐related prooxidative enzymes (iNOS and COX‐2) in ischemic brain. Moreover, T4 down‐regulated the phosphorylation of p38 and prevented injury‐induced increase of PKCδ. These results revealed that T4 has a promising therapeutic effect in ischemic stroke treatment protecting the brain from I/R injury, probably by its anti‐apoptotic, and anti‐inflammatory mechanism.
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