miR-155-5p accelerates cerebral ischemia-reperfusion inflammation injury and cell pyroptosis via DUSP14/ TXNIP/NLRP3 pathway
Objective: Cerebral ischemia/reperfusion (I/R) injury is stimulated by blood restoration after ischemic stroke. Inflammatory response and inflammasome activation exerted vital functions in the development of cerebral I/R injury. miR-155-5p regulates inflammatory response in some diseases, while its role in inflammatory response and inflammasome activation of cerebral I/R injury development is unclear. Hence, the research focuses on investigating if miR-155-5p attenuate cerebral I/R injury via regulating inflammatory response and inflammasome activation and exploring the potential mechanism. Methods: The oxygen-glucose deprivation/reoxygenation (OGD/R) model and the middle cerebral artery occlusion (MCAO) model were constructed. Cell viability and cytotoxicity were reflected by CCK-8 assay and LDH activity. The inflammatory cytokines secretion was determined using ELISA assay. Brain tissue infarction was evaluated using TTC staining. Results: miR-155-5p, Thioredoxin Interacting Protein (TXNIP) and NLR Family Pyrin Domain Containing 3 (NLRP3) were highly expressed in OGD/R model and MCAO rats. Knockdown of miR-155-5p alleviated cell injury, cell inflammation, and cell pyroptosis stimulated by OGD/R. Besides, miR-155-5p regulated TXNIP/NLRP3 pathway through modulating Dual-Specificity Phosphatase 14 (DUSP14) expression. Furthermore, knockdown of miR-155-5p improved brain tissue infarction and inhibited inflammation response and cell pyroptosis of MCAO rats. Conclusion: Knockdown of miR-155-5p attenuated I/R inflammation and cell pyroptosis of cerebral via modulating DUSP14/TXNIP/NLRP3 pathway. These findings may provide a promising strategy to attenuate cerebral I/R injury.
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