The First Department of Otolaryngology, Children's Hospital, Shandong University, No.23976, Jingshi Road, Jinan City, Shandong Province, 250022, China.
The First Department of Otolaryngology, Jinan Children's Hospital, No.23976, Jingshi Road, Shandong Province, Jinan City, 250022, China.
Appl Biochem Biotechnol. 2022 Aug;194(8):3483-3493. doi: 10.1007/s12010-022-03837-4. Epub 2022 Apr 2.
Herpes simplex virus type 1 (HSV-1) results in the development of Bell's pals but still, the pathophysiology of the facial nerve paralysis is still not fully studied. The main objective is to establish an animal model of type 1 herpes simplex virus (HSV-1)-induced face paralysis in the mouse and to investigate the pattern of changes in intercellular adhesion molecule -1(ICAM-1) expression in the facial nucleus of the brain stem in mice with facial paralysis as well as the effects of glucocorticoids on intercellular adhesion molecule -1(ICAM-1) expression. A total of 170 4-week-old Balb/c male mice were randomly divided into the virus inoculation group (n = 135), saline control group (n = 26), and blank control group (n = 9). Mice in the virus inoculation group that showed facial paralysis were divided into A, B, and C subgroups. The A group did not receive any treatments, the B group received methylprednisolone sodium succinate (MPSS) intervention, and the C group received MPSS + RU486 treatment. The mouse model of facial paralysis was established by inoculating HSV-1 to the skin at the back of the ears. The facial nerve function of mice was assessed, and real-time PCR and western blot were used to assess ICAM-1 expression in the facial nucleus of the brain stem in mice with facial paralysis after drug intervention. In the virus inoculation group, 95 mice (55.88%) showed varying degrees of facial paralysis symptoms within 2-5 days after inoculation. The ICAM-1 gene and protein expression levels remained at low levels in the facial nucleus of the brain stem of mice in the saline group, which showed no significant difference compared to the normal control group (P > 0.05). However, for mice of the virus inoculation group, ICAM-1 expression increased at 6 h after the occurrence of facial paralysis and peaked after 2 days, differing significantly from the blank control group (P < 0.01). ICAM-1 expression subsequently decreased gradually. In the HSV-1 + MPSS group, ICAM-1 protein expression decreased significantly on the 2 day after facial paralysis. In the HSV-1 + MPSS + RU486 group, MPSS inhibition of ICAM-1 protein expression was reduced. The results suggested that ICAM-1 is involved in the pathological processes by which HSV-1 induces facial paralysis in mice, and the treatment effects of MPSS for Bell's palsy can be achieved by the inhibition of MCP-1.
单纯疱疹病毒 1 型（HSV-1）可导致贝尔面瘫，但面神经麻痹的病理生理学仍未完全研究清楚。主要目的是建立 1 型单纯疱疹病毒（HSV-1）诱导的小鼠面瘫动物模型，并研究面瘫小鼠脑干面神经核细胞间黏附分子-1（ICAM-1）表达的变化模式，以及糖皮质激素对细胞间黏附分子-1（ICAM-1）表达的影响。共 170 只 4 周龄雄性 Balb/c 小鼠随机分为病毒接种组（n=135）、生理盐水对照组（n=26）和空白对照组（n=9）。病毒接种组中出现面瘫的小鼠分为 A、B、C 亚组。A 组未接受任何治疗，B 组接受甲泼尼龙琥珀酸钠（MPSS）干预，C 组接受 MPSS+RU486 治疗。通过在耳后皮肤接种 HSV-1 建立面瘫小鼠模型。评估小鼠面神经功能，药物干预后面瘫小鼠脑干面神经核 ICAM-1 表达采用实时 PCR 和 Western blot 检测。病毒接种组中，95 只（55.88%）小鼠在接种后 2-5 天出现不同程度的面瘫症状。生理盐水组小鼠脑干面神经核中 ICAM-1 基因和蛋白表达水平均处于较低水平，与正常对照组相比无显著差异（P＞0.05）。然而，对于病毒接种组的小鼠，面瘫发生后 6 小时 ICAM-1 表达增加，2 天后达到峰值，与空白对照组相比差异有统计学意义（P＜0.01）。随后 ICAM-1 表达逐渐下降。在 HSV-1+MPSS 组中，面瘫后第 2 天 ICAM-1 蛋白表达明显下降。在 HSV-1+MPSS+RU486 组中，MPSS 对 ICAM-1 蛋白表达的抑制作用降低。结果提示，ICAM-1 参与 HSV-1 诱导小鼠面瘫的病理过程，MPSS 通过抑制 MCP-1 治疗贝尔面瘫。
