Flurbiprofen axetil protects against cerebral ischemia/reperfusion injury via regulating miR-30c-5p and SOX9

The modulatory mechanism of flurbiprofen axetil (FPA) by which it relieves cerebral ischemia/reperfusion (I/R) injury (CIRI) is still obscure. In the present work, adult male Sprague-Dawley (SD) rats were pre-treated with FPA before the construction of a rat model of CIRI. Longa's scoring method and dry-wet method were employed to examine the neurological function and brain water content of the rats. MiR-30c-5p, SOX9, AQP4, SOX9, NF-kappa B, and p-NF-kappa B expression levels in the brain tissues of the rats were examined by qRT-PCR or Western blot. ELISA was executed to evaluate the IL-10, IL-6, and TNF-alpha levels in the serum of rat. SOD and MDA levels in rat brain homogenates were also examined to indicate the oxidative stress. Hematoxylin-eosin (HE) staining was used to examine the pathological changes of the brain tissues. Dual-luciferase reporter gene experiment was implemented to validate the binding relationship between miR-30c-5p and SOX9. In the present work, compared with the rats with CIRI, FPA pre-treatment attenuated neurological injury, cerebral edema, oxidative stress, inflammatory response, and cerebral pathological changes in the rat model with CIRI. FPA up-modulated miR-30c-5p expression. SOX9 was a downstream target of miR-30c-5p. In conclusion, FPA ameliorates CIRI through up-modulating miR-30c-5p expression and reducing SOX9 expression.

Automated summary

The study found that pre-treatment with flurbiprofen axetil (FPA) can alleviate neurological injury, cerebral edema, oxidative stress, inflammatory response, and cerebral pathological changes in a rat model of cerebral ischemia/reperfusion injury (CIRI). FPA improves CIRI by up-regulating miR-30c-5p expression and reducing SOX9 expression.