The Alterations And Significant Of Monocyte Chemoattractant Protein-land Intercellular Adhesion Molecule-1 In Mouse Brainstem During Herpes Simplex Virus Type 1-induced Facial Palsy

Objectives:To establish an animal model of facial nerve palsy in mice induced by herpes simplex virus type 1 (HSV-1) infection in order to explore the changes of monocyte chemoattractant protein-1 (MCP-1) in the mouse brainstem during the development of facial paralysis induced by HSV-1 and the effect of glucocorticoid on the expression of MCP-1.Methods:170 four-weeks Balb/c male mice were randomly divided into virus inoculated group (135 mice), saline group (26 mice) and normal control group (9 mice). HSV-1 was inoculated into the surface of posterior auricle of mouse to establish a paralyzed animal model. The paralyzed mice in virus inoculated group were further divided into three subgroups (groups A, B and C). Drugs for intervention were methylprednisolone sodium succinate (MPSS) and glucocorticoid receptor blocking agent (RU486). No drug intervention was performed in group A; mice in group B were injected daily with MPSS for 2 days and in group C, mice were injected daily with combination of MPSS and glucocorticoid receptor blocker (RU486) for 2 days. The expression of MCP-1 in the facial nucleus of brainstem were detected respectively by quantitative real-time polymerase chain reaction, western blot and immunohistochemistry.Results:1. Of the 170 mice subjected to retroauricular inoculation with HSV-1, 95(55.88%) developed unilateral facial paralysis between 2 and 5 days.65 mice of the 95 paralyzed mice were involved in experiment Part 1 as facial paralysis group.2. The expression of MCP-1 protein in the facial nucleus of brainstem increased dramatically compared with the control group by immunohistochemistry (P <0.05).3. In the saline group, the level of MCP-1 mRNA in the facial nucleus of brainstem were low, and compared with the control group there were no significant difference between them(P> 0.05). In facial paralysis group, the expression of MCP-1 mRNA increased at 6h post-induction of facial paralysis, and was peaked at 2d (P <0.01), then the level of MCP-1 gradually decreased and tended to be normal (P> 0.05).4. In the saline group, the level of MCP-1 protein in the facial nucleus of brainstem were low, there were no significant difference between them compared with the control group (P> 0.05). In facial paralysis group, the expression of MCP-1 protein increased at 6h post-induction of facial paralysis, and was peaked at 2d (P <0.01), then the level of MCP-1 gradually decreased and was higher than that of the control group (P<0.05).5. At the time point of 2 days, the expressions of MCP-1 protein in paralyzed mice with administration of MPSS decreased dramatically compared with those paralyzed mice without any administration (P<0.05).6. The expression of MCP-1 protein of paralyzed mice was inhibited by MPSS, and the inhibition could be blocked by RU486 (P<0.05). At the time point of 2 days, the level of MCP-1 protein in paralyzed mice with combination of MPSS and RU486 with administration of MPSS was higher than those of normal control (P< 0.05).Conclusions:1. MCP-1 is involved in the pathogenesis of facial palsy induced by HSV-1.2. MPSS could effectively inhibit the expression of MCP-1 that may contribute to attenuate HSV-1-mediated nervous system damage.Objectives:To explore the changes of intercellular adhesion molecule-1 (ICAM-1) in the mouse brainstem during the development of facial paralysis induced by HSV-1 and the effect of glucocorticoid on the expression of ICAM-1.Methods:The specimens from A, B, C groups and the normal control group in the first part of the experiment were included in this part of the experimental study. The expression of ICAM-1 in the facial nucleus of brainstem were detected respectively by quantitative real-time polymerase chain reaction, western blot and immunohistochemistry.Results:l.The expression of ICAM-1 protein in the facial nucleus of brainstem increased dramatically compared with the control group by immunohistochemistry (P <0.05).2. In the saline group, the level of ICAM-1 mRNA in the facial nucleus of brainstem were low, and compared with the control group there were no significant difference between them(P> 0.05). In facial paralysis group, the expression of ICAM-1 mRNA increased at 6h post-induction of facial paralysis, and was peaked at 2d (P<0.01), then the level of ICAM-1 gradually decreased and tended to be normal (P> 0.05).3. In the saline group, the level of ICAM-1 protein in the facial nucleus of brainstem were low, there were no significant difference between them compared with the control group (P> 0.05). In facial paralysis group, the expression of ICAM-1 protein increased at 6h post-induction of facial paralysis, and was peaked at 2d (P <0.01), then the level of ICAM-1 gradually decreased and was higher than that of the control group (P<0.05).4. At the time point of 2 days, the expressions of ICAM-1 protein in paralyzed mice with administration of MPSS decreased dramatically compared with those paralyzed mice without any administration (P<0.05).5. The expression of ICAM-1 protein of paralyzed mice was inhibited by MPSS, and the inhibition could be blocked by RU486 (P<0.05). At the time point of 2 days, the level of ICAM-1 protein in paralyzed mice with combination of MPSS and RU486 with administration of MPSS was higher than those of normal control (P< 0.05).Conclusions:1. ICAM-1 is involved in the pathogenesis of facial palsy induced by HSV-12. MPSS could effectively inhibit the expression of ICAM-1 that may contribute to attenuate HSV-1-mediated nervous system damage.Objectives:To explore the effect of Bindarit, an inhibitor of monocyte chemotactic protein synthesis, on the expression of monocyte chemotactic protein-1 and intercellular adhesion molecule-1 in the mouse brainstem during herpes simplex virus type 1-induced facial palsy and to determine whether there is a correlation between MCP-1 and ICAM-1.Methods:Thirty facial paralyzed mice induced by herpes simplex virus type 1 and the normal control group in the first part of the experiment were included in this part of the experimental study. The mice were injected daily with Bindarit for 2 days. The expression of MCP-1 and ICAM-1 protein in the facial nucleus of brainstem were detected by western blot.Results:1. At the time point of 2 days, the expression of MCP-1 protein in paralyzed mice was inhibited by Bindarit (P<0.05).2. At the time point of 2 days, the level of ICAM-1 protein in paralyzed mice with Bindarit was decresed dramatically (P< 0.05). The variation tendency of MCP-1 and ICAM-1 was in the same.Conclusions:1. Bindarit could decresed dramatically the expression of MCP-land ICAM-1 protein in the facial nucleus of brainstem paralyzed mice caused by HSV-1.2. There is a correlation between MCP-1 and ICAM-1.