| Popis: |
This study was conducted to investigate the mechanism of facial nerve recovery through Toll-like receptor 2 (TLR2)/nuclear factor kappa B (NF-κB) after facial nerve trunk damage. Facial nerve surgery was performed on rats to establish a paralyzed animal model with or without intraperitoneal (i.p.) injection of Pam3CSK4 (TLR2 agonist). All nucleic acids were extracted using nanometer magnetic beads. At 1, 4, 7, 10, 13, and 16 days after the surgery, the score of the blink reflex, the motion of vibrissae, and the motion of nose were analyzed to assess the function of facial nerves. Evaluated using transmission electron microscopy (TEM) and immunofluorescence staining (IF), Morphological changes in facial nerve and brainstem were analyzed. The expressions of TLR2 and NF-κB p65 in the brainstem were detected by quantitative Reverse Transcription-Polymerase Chain Reaction (RT-PCR), western blotting, and IF. TEM revealed that the facial nerve fiber diameter was shortened, and the organelle was swollen and demyelinated in the operation group. The IF results revealed that the expressions of NF-κB p65 and TLR2 in the brainstem were increased significantly in the operation group together with the control group. RT-PCR demonstrated that the mRNA expressions of TLR2 and NF-κB p65 in the brainstem were low in the control group, as well as in the sham group, whereas there were significant increases in the mRNA expressions of TLR2 and NF-κB p65 in the operation group. Western blotting revealed a significant increase in the expression of TLR2 protein after the surgery compared to that in the control group. After subjecting the rats to facial nerve surgery and i.p. injection of Pam3CSK4, the protein expressions of TLR2 and NF-κB p65 were upregulated dramatically in the Pam3CSK4-operation group compared to that in the control group and were also significantly increased than those in the operation group. Both facial nerve dysfunction caused due to facial nerve surgery (exacerbated by co-treatment with Pam3CSK4) and the expressions of NF-κB p65 and TLR2 were increased significantly. TLR2 might be an innovative gene target and a novel option for the clinical applications of facial paralysis immunotherapy. |
