| First Author | Liu W | Year | 2015 |
| Journal | Neuroscience | Volume | 289 |
| Pages | 251-61 | PubMed ID | 25595974 |
| Mgi Jnum | J:221436 | Mgi Id | MGI:5639168 |
| Doi | 10.1016/j.neuroscience.2014.12.062 | Citation | Liu W, et al. (2015) Activation of NF-kappaB signaling pathway in HSV-1-induced mouse facial palsy: Possible relation to therapeutic effect of glucocorticoids. Neuroscience 289:251-61 |
| abstractText | It has been documented that infection of herpes simplex virus type 1 (HSV-1) contributes to the initiation of Bell's palsy. However, the exact mechanisms responsible for this disorder have not been fully elucidated to date. A mouse model of facial palsy induced by HSV-1 provides an opportunity to investigate the alteration in activities of nuclear factor-kappa B (NF-kappaB) and its consequent effect on two key inflammatory factors, i.e., tumor necrosis factor (TNF)-alpha and cyclooxygenase-2 (COX-2), as well as the effect of glucocorticoids (GCs) in this work. I-kappa B (IkappaB)-alpha phosphorylation and NF-kappaB nuclear translocation were measured by western blotting, and NF-kappaB/DNA binding activity was assessed by electrophoretic mobility shift assay (EMSA). Results showed the IkappaB-alpha phosphorylation and degradation as well as NF-kappaB activation in a time-dependent manner. The expression of TNF-alpha and COX-2 were determined by real-time polymerase chain reaction (PCR), western blotting and/or enzyme-linked immunosorbent assay (ELISA) respectively. Concomitant with the activation, the expression and secretion of TNF-alpha and COX-2 were rapidly induced in HSV-1-infected paralyzed mice. Conversely, the activation of NF-kappaB and up-regulation of TNF-alpha and COX-2 were blocked by pretreatment with NF-kappaB inhibitor pyrrolidine dithiocarbamate (PDTC) before being inoculated with HSV-1 to mice. In addition, GCs inhibited the nuclear translocation and DNA binding activity of NF-kappaB via inhibiting IkappaB-alpha degradation. Meanwhile, TNF-alpha production and COX-2 expression were significantly reduced by GCs. In conclusion, HSV-1 inoculation induced the activation of NF-kappaB, expression and secretion of TNF-alpha and COX-2 in the facial paralyzed mice, while, glucocorticoid effectively down-regulated TNF-alpha and COX-2 expression in HSV-1-induced paralyzed mice. |
