| Abstract: | AIM To investigate the role of mast cells in the pain of adjuvant arthritis (AA) in mice induced by complete Freund's adjuvant (CFA). METHODS The animals were divided into 4 groups: normal control group (control group), AA model group (model group) and AA model + cromolyn sodium (CS) group (CS group), AA model + mast cell lacking group (W-4Bao group), with 6 mice in each group. The animals in the first 3 groups were C57BL/6 mice, while those in W-4Bao group were KitW-4Bao mice lacking of mast cells. The pain model of chronic AA was induced by intraplantar injection of CFA into the right hind paws of the mice, while the mice in control group was injected with saline. One day after CFA injection, the mice in CS group were intraperitoneally injected with CS (20 mg/kg), and those in other groups received an equal volume of saline once a day for 14 d. The paw edema, paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were evaluated at 0, 1, 3, 7, 10 and 14 d after CFA injection. The mouse right ankle joint was harvested after 14 d for HE and toluidine blue staining, and the concentrations of histamine, tryptase, substance P (SP), calcitonin gene-related peptide (CGRP) were detected by ELISA. RESULTS One day after CFA injection, the inflammation of the right hind paw in model group was more serious compared with control group, and the PWT and PWL were notably decreased (P<0.05). In addition, the numbers of mast cells and degranulated mast cells were increased obviously, and the concentrations of histamine, tryptase, SP and CGRP were increased (P<0.05). However, compared with model group, hyperalgia and the release of neuropeptides in CS group and W-4Bao group were significantly decreased (P<0.05). CONCLUSION The activation of mast cells promotes the pain of AA in mice, and its mechanism may be associated with the release of neuropeptides and relevant inflammatory factors. |
