Effect of CYLD Overexpression on NF-κB Signaling Pathway after Oxygen-Glucose Deprivation/Reoxygenation in Rat Primary Cortical Neurons
Zhu Jun, Xu Hongbei, Zhou Xueling, Lu Wenhao, Luo Yong*
Stroke is one of the most leading cause of years of life lost (YLLs) in our population. After cerebral ischemia/reperfusion in ischemic stroke, there are many complex pathophysiological mechanisms in the damaged brain tissue. The inflammatory response in which nuclear factor-κB (NF-κB) signaling pathway participates is one of the most important mechanisms. Studies have shown that cylindromatosis (CYLD) can regulate NF-κB signaling pathway. However, can up-regulation of CYLD expression regulate the NF-κB signaling pathway in neurons after oxygen-glucose deprivation/reoxygenation? How to? So far no study has been reported yet, it needs to be researched. Our study up-regulates the expression of CYLD in neurons to investigate the effect of CYLD on NF-κB signaling pathway after oxygen-glucose deprivation/reoxygenation (OGD/R) in rat primary cortical neurons. Primary cortical neurons were infected by lentiviral vector-mediated overexpression of CYLD. Neurons were identified by immunofluorescence. The protein levels and mRNA levels were detected respectively by Western blot and RT-qPCR to confirm the expression of CYLD. Cell viability was detected by CCK-8 assay. The protein levels of p-IκBα were detected by Western blot. The mRNA levels of NF-κB p65 were detected by RT-qPCR. The results indicated that lentiviral vector-mediated CYLD overexpression can efficiently upregulate CYLD expression in neurons. After OGD/R, neuronal viability was enhanced significantly in CYLD-overexpressing neurons compared to control neurons. Meanwhile, the expression of p-IκBα and NF-κB p65 were decreased. The results suggested that overexpression of CYLD in primary cortical neurons could attenuate neuronal damage and inhibit the NF-κB signaling pathway induced by oxygen-glucose deprivation/reoxygenation.
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