Aim
The aim was to study the role of Rph3A in neuronal injury induced by cerebral ischemia-reperfusion.
Conclusion
The increase in Rph3A in the brain penumbra may be an endogenous protective mechanism against ischemia-reperfusion injury, which is mainly dominated by astrocytes.
Methods
The protein and mRNA levels of Rph3A in penumbra were detected by Western blot. The localization of Rph3A in different cell types in penumbra was detected by immunofluorescence. Apoptosis in the brain was detected by TUNEL staining. We tested neurobehavioral evaluation using rotarod test, adhesive-removal test, and Morris Water maze test. We examined the expression and localization of Rph3A in cultured neurons and astrocytes in vitro by Western blot and ELISA, respectively.
Results
The mRNA and protein levels of Rph3A had significantly increased in brain penumbra of the rat MCAO/R model. Rph3A was mainly distributed in neurons and astrocytes and was significantly increased by MCAO/R. We downregulated Rph3A and found that it further worsened the cerebral infarct, neuronal death and behavioral, cognitive, and memory impairments in rats after MCAO/R. We also found that ischemia-reperfusion upregulated the in vitro protein level and secretion of Rph3A in astrocytes but led to a decrease in the protein level of Rph3A in neurons.