Neurological research · 2012
The alterations of inducible nitric oxide synthase in the mouse brainstem during herpes simplex virus type 1-induced facial palsy.
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Mao Yanyan, Fan Zhaomin, Han Yuechen, Liu Wenwen, Xu Lei, Jiang Zhen, Li Jianfeng, Wang Haibo
Аннотация
OBJECTIVE: We sought to study the alterations of inducible nitric oxide synthase (iNOS) in the mouse brainstem during facial paralysis induced by herpes simplex virus type 1 (HSV-1) and the inhibitory effects of glucocorticoids.
METHODS: HSV-1 was inoculated into the surface of posterior auricle of mouse to set up an animal model. The paralyzed mice were divided in three groups as detailed in text. Mice, in one group, were killed at different time points and, in other two groups, were injected daily for 2 days with methylprednisolone sodium succinate (MPSS) or with combined administration of MPSS and glucocorticoid receptor blocker (RU486). Morphological changes were evaluated by means of hematoxylin and eosin (H&E) staining and improved trichrome staining. The expression and location of iNOS in the facial nucleus of brainstem was detected by reverse transcription-polymerase chain reaction (RT-PCR), western blot, and immunohistochemistry.
RESULTS: After inoculated by HSV-1, 49·09% of mice developed unilateral facial paralysis. Injuries in response to HSV-1 infection in the facial nerves and facial nucleus of paralyzed mice were observed by morphological methods. Besides, we found that iNOS was present in normal glial cells and motor neurons at low levels and was upregulated dramatically after facial paralysis, which could be inhibited by MPSS. RU486, a glucocorticoid receptor inhibitor, could block the inhibitory effects of MPSS.
DISCUSSION: The present study demonstrates that the enhanced activity of iNOS in the early phase represents an important mechanism in HSV-1-induced facial paralysis. MPSS can effectively attenuate HSV-1-mediated damages in nerve system, which is closely associated to its inhibitory effect on expression of iNOS.
METHODS: HSV-1 was inoculated into the surface of posterior auricle of mouse to set up an animal model. The paralyzed mice were divided in three groups as detailed in text. Mice, in one group, were killed at different time points and, in other two groups, were injected daily for 2 days with methylprednisolone sodium succinate (MPSS) or with combined administration of MPSS and glucocorticoid receptor blocker (RU486). Morphological changes were evaluated by means of hematoxylin and eosin (H&E) staining and improved trichrome staining. The expression and location of iNOS in the facial nucleus of brainstem was detected by reverse transcription-polymerase chain reaction (RT-PCR), western blot, and immunohistochemistry.
RESULTS: After inoculated by HSV-1, 49·09% of mice developed unilateral facial paralysis. Injuries in response to HSV-1 infection in the facial nerves and facial nucleus of paralyzed mice were observed by morphological methods. Besides, we found that iNOS was present in normal glial cells and motor neurons at low levels and was upregulated dramatically after facial paralysis, which could be inhibited by MPSS. RU486, a glucocorticoid receptor inhibitor, could block the inhibitory effects of MPSS.
DISCUSSION: The present study demonstrates that the enhanced activity of iNOS in the early phase represents an important mechanism in HSV-1-induced facial paralysis. MPSS can effectively attenuate HSV-1-mediated damages in nerve system, which is closely associated to its inhibitory effect on expression of iNOS.