Objective: To investigate the effects of mast cells (MCs) and the relationship between the signal pathway including transient receptor potential vanilloid receptor 1 (TRPV1) and extracellular-regulated kinase (ERK) and MCs in rat models of visceral hyperalgesia triggered by infection and stress.
Methods: MCs deficient rats (WsRC Ws/Ws, Ws/Ws) and control (WsRC+/+, +/+) rats were exposed to Trichinella spiralis (T.spiralis) post-infection (PI) or submitted to acute cold restraint stress (ACRS). Visceral sensitivity was measured using the abdominal withdrawal reflex (AWR) score. Levels of TRPV1 and phosphorylated ERK1/2 (pERK1/2) proteins in L6S1 spinal cord segments were determined by Western blotting.
Results: Compared with control group (3.7±0.09), visceral hyperalgesia was enhanced in PI (2.52±0.13), ACRS (2.28±0.17) and PI+ACRS (2.25±0.12) groups of +/+ rats, P< 0.05. In Ws/Ws rats, compared with control group (3.25±0.20), visceral hyperalgesia was enhanced in PI (2.87± 0.14) and PI+ACRS (2.50±0.27) groups, P< 0.05, but not in ACRS group (2.97±0.22). Compared with control group (0.090±0.009), a significant increase of TRPV1 was observed in PI (0.121±0.012), ACRS (0.122±0.008) and PI+ACRS (0.129±0.008) in spinal cord of +/+ rats, P< 0.05. However, compared with control group (0.106±0.012), a significant increase of TRPV1 was observed in PI (0.140±0.008, P< 0.05) and PI+ACRS (0.156±0.010, P< 0.01) groups but not in ACRS group(0.132±0.014)in spinal cord of Ws/Ws rats. Compared with control group (0.58± 0.03), a significant increase of pERK1/2 was observed in PI (0.72±0.04), ACRS (0.75±0.04) and PI+ACRS (0.78± 0.01) in spinal cord of +/+ rats, P< 0.01. However, compared with control group (0.59±0.04), a significant increase of pERK1/2 was observed in PI (0.72±0.04, P< 0.05) and PI+ACRS (0.74±0.04, P< 0.05) groups but not in ACRS group(0.132±0.014)in spinal cord of Ws/Ws rats.
Conclusion: The visceral hyperalgesia was enhanced in rats induced by T.spiralis infection and ACRS, however, the increased visceral hyperalgesia in rats induced by ACRS was dependent on MCs. The signal pathway proteins including TRPV1 and pERK1/2 were increased in rats induced by T.spiralis infection and ACRS, but the sensitizing TRPV1 or mobilizing ERK1/2 phosphorylation via a MCs-dependent mechanism plays an important role in ACRS-induced visceral hyperalgesia rats.