RESEARCH ON AQP1 PARTICIPATES IN THE EXPRESSION REGULATION MECHANISM OF FACIAL NERVE EDEMA BY ACTIVATING THE MAPK SIGNALING PATHWAY

Mengying Cao¹, Lixing Dai¹, Chang Gao^2*

¹Department of General Practice, the Third People's Hospital of Hubei Province, Wuhan 430033, Hubei Province, China - ²Department of Neurology, the Third People's Hospital of Hubei Province, Wuhan 430033, Hubei Province, China

Objective: To explore the expression and regulation mechanisms of aquaporin 1 (AQP1) in facial edema by activating the mitogen-activated protein kinase (MAPK) signal pathway. 

Method: The Schwann cell line RSC96 was used to establish a model of hypoxia. After successful modeling, the cell viability, protein expression level of AQP1 at 0h, 1h, 3h, 6h, and the protein expression levels of MAPKs (p-p38, p38, p-ERK, extracellular signal-regulated kinase [ERK], p-JNK, and c-Jun N-terminal kinase [JNK]) signaling pathway at 0min, 15min, 30min, 45min, and 60min were compared in each group. The remaining RSC96 cell hypoxia models were randomly divided into the control group, the hypoxia group, the hypoxia + SB group, the hypoxia + U group, and the hypoxia + SP group. The control group cells were given 5% CO₂ and 95% air intervention. The hypoxia group cells were treated with 2% O₂, 5% CO₂, 93% N₂ and placed in a hypoxic box for one hour. The hypoxia + SB group cells were treated with 2% O₂, 5% CO₂, 93% N₂, and 10 μmol p38 signal Intervention by pathway inhibitor SB20358 and then placed in a hypoxic box for one hour. The hypoxia + U group cells were treated with 2% O₂, 5% CO₂, 93% N₂ and 10 μmol ERK signaling pathway inhibitor U10126 and placed Cultured in a hypoxic box for one hour. The hypoxia + SP group cells were treated with 2% O₂, 5% CO₂, 93% N₂, and 10 μmol JNK signaling pathway inhibitor SP00125 and placed in a hypoxic box for one hour. The expression levels of AQP1, p-p38, p38, p-ERK, ERK, p-JNK, and JNK protein were compared in each group of cells. 

Results: The activity of RSC96 cells at 6h of hypoxia was significantly lower than at 0h of hypoxia (P<0.05). There was no significant difference in the expression level of AQP1 protein in RSC96 cells at 1 h of hypoxia compared with 0 h (P>0.05). The expression level of AQP1 protein in RSC96 cells was significantly higher than that of 0h hypoxia at 3h and 6h (P<0.05). The expression level of AQP1 protein in RSC96 cells was significantly higher than that at 3h at 6h hypoxia (P<0.05). The expression levels of p-p38, p-ERK and p-JNK protein in RSC96 cells at 15min, 30min, 45min, 60min of hypoxia were significantly higher than that of hypoxia at 0min, which was time-dependent (P<0.05). The expression levels of AQP1 and p-p38 protein in RSC96 cells in the hypoxia group were significantly higher compared to the control group (P<0.05). The expression levels of AQP1 and p-p38 protein in RSC96 cells in the hypoxia + SB group were significantly lower than the levels in the hypoxia group (P<0.05). There was no significant difference in the expression level of p38 protein in RSC96 cells in each group (P>0.05). The expression of AQP1 and p-ERK protein in RSC96 cells in the hypoxia group was significantly higher compared to the control group (P<0.05). Additionally, the expression of AQP1 and p-ERK protein in RSC96 cells of the hypoxia + U group was significantly lower than the levels of the hypoxia group (P<0.05). There was no significant difference in the expression level of ERK protein in RSC96 cells in each group (P>0.05). The expression of AQP1 and p-JNK protein in RSC96 cells in the hypoxia group was significantly higher than the levels in the control group (P<0.05), and the expression of p-JNK protein in RSC96 cells in the hypoxia + SP group was significantly lower compared to the hypoxia group (P<0.05). There was no significant difference in the expression level of JNK protein in RSC96 cells between each group (P>0.05). 

Conclusion: AQP1 can regulate facial nerve edema, and its mechanism of action may be achieved by activating the MAPK signaling pathway.