| Bell's palsy is an acute unilateral paralysis of the facial nerve, and is considered the most common cause of facial nerve paralysis. Its cause is unknown but it affects 11-40 people per 100 000 in the population per annum, most commonly in the age group 30-45. The condition is most common among pregnant women and people who have diabetes, influenza, a cold or some other upper respiratory ailment. Although most recover, as many as 30% of people recovery with continuing facial disfigurement, psychological difficulties and sometimes facial pain. In the absence of an established pathophysiology:swelling and entrapment of the nerve. Some studies suggested that the mayority of Bell's palsy cases might be caused by reactivation of latent HSV-1 infection in the geniculate ganglion. Since HSV-1 is highly neurotropic, it travels retrogradely along motor nerves to the sensory ganglia where latency is established. Histopathological study of the intratemporal portion of the facial nerve showed that the virus replicated profusely in the neurons of the geniculate ganglion, and that the motor fibers of the facial nerve underwent demyelination in Bell's palsy. Facial nerve consists of motor and sensory fibers. Sensorial neurons of facial nerve, innervating the posterior auricle, are located in the geniculate ganglion. Therefore, it is considered that auricular scratch in combination with immunosuppression promotes the reactivation of the latently infected HSV-1 in the geniculate ganglion. Replicated and released viruses must infect Schwann cells adjacent to the facial motor nerve, causing demyelination. Subsequently, vigorous destruction of the facial nerve, which induces an inflammatory reaction in the narrow facial canal in the temporal bone, may exacerbate the paralysis. Glucocorticoids are the most effective anti-inflammation drugs available for the treatment many inflammtory and immune diseases. Glucocorticoids diffuse across the cell membrane and bind to glucocorticoid receptors(GR) in the cytoplasm. Upon ligand binding. GR are activated and released from chaperone proteins and rapidly translocate to the nuleus where they exert their molecular effects. Recently, there is no clear program for the treatment of Bell's palsy. The clinical data indicate that glucocorticoids have a positive effect for the prognosis of Bell's palsy. In addition, some scholars have found that glucocorticoids have large extent dependent of on their concentration for the regeneration of nerve fibers stimulated and nerve degeneration,nerve protection and regeneration. However, the exact mechanism is still not clear for treatment of Bell's palsy, the timing, dose, treatment options of their medication is not precise, more personal experience for treatment. Established animal model of facial paralysis caused by HSV-1, the expression of glucocorticoid receptor is researched in facial motor cortex and facial nucleus in mice infected with HSV-1, and reveal paralysis therapeutic mechanism for action of glucocorticoid on viral facial, and guide rational clinical treatment of Bell's palsy, and prevent the phenomenon of hormone resistance instructive.Objective To establish an animal model of facial nerve palsy in mice induced by herpes simplex virus type 1 (HSV-1) infection so as to investigate the expression of glucocorticoid receptor (GR) in in the motor cortex and facial nucleus.Methods A total of 89 four-week-old female Bulb/c mice were selected in this work. These animals were randomly divided into two groups, i.e., the control group without any intervention and the experimental group, in which 25μL HSV-1 was inoculated into the right auricle after scratching the surface of bilateral auricles with a 26 gauge needle. The tissues were taken out at 6 h,12 h,24 h,48 h,72 h, and 7 d after the appearance of facial nerve palsy. Western blot and immunohistochemistry were used to detect the level of GR protein, RT-PCR was used to measure the level of GR mRNA.Results The incidence of facial nerve palsy was 52.3% among the 81 inoculated animals. GR was localized in facial nucleus.. GR mRNA expression in experimental group was slightly decreased after facial nerve palsy in the motor cortex and facial nucleus, sharply declined at 6 h, showing a significant difference compared with control group (P<0.05). The expression gradually reached a peak at 48 h, having a significant difference compared with control group (P<0.01). The expression eventually returned to the baseline level at and after 7 d, but, not showing a notable difference between the two groups (P>0.05).GR protein expression in experimental group was similar to GR mRNA.Conclusions GR expression in response to HSV1 infection appears in a time-depend manner, indicating that GR expression level is closely related to the progress in HSV1-induced facial nerve palsy. Our findings may be of import clinic implication in the rational use of glucocorticoid and attenuation of the phenomenon of hormone resistance in treatment of Bell's facial paralysis. |
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