The Study On The Mechanisms Of Glial Cells In Visceral Hyperalgesia In Rats With IBS

Background:Irritable bowel syndrome is a chronic intestinal function disease,In special of hyperalgesia is its characterized.Visceral hypersensitivity is one of the pathogenesis,and be paid more attention.But the neuronal mechanisms are unclear.Taken together,it is more important to investigate the pathogenesis of IBS. Recent studies have indicated an important role of glial cells in the visceral hypersensitivity of IBS. Particularly glial cells in dorsal commissual nucleus that dominant left colon in the spinal may have closely related visceral hypersensitivity of IBS, it has become a hot issue of the current study.Objective:By using the trichinella gavage method to set up the animal models of IBS in rats infected with Trichinella spiralis, Injected some water into balloon into the colon of model rats and inhibitor SB203580 injection by spinal catheter. To investigate the changes of electro-activity of the rectus abdominis in irritable bowel syndrome(IBS) rats, the expression of NMDAR and CGRP and P38 in dorsal horn of the spinal cord of rats with IBS, and the activation of microglial cells in dorsal commissural nucleus(DCN), and to provide a theoretical basis for visceral hyperalgesia of the rats with IBS.Methods:Trichinella suspension by gavage to establish IBS model, to observed by electrophysiological methods in normal rats and changes in IBS rat rectus abdominis muscle; Observed by immunohistochemistry between the posterior horn of the sacral NMDAR, P38, CGRP, ERK, and sacral joint nuclear in the expression of microglia.ResultsThe electro-activity of the rectus abdominis, the expression of NMDAR, CGRP, P38, ERK and activation of microglia of the sacral joint nuclear were significantly enhanced in IBS rats with colon stimulate than the normal and non-stimulation IBS rats groups(P<0.01). The expansion of IBS rat with colon stimulate sacral the P38, ERK expression was significantly increased compared with normal rats in the posterior horn, while OX42 expression was significantly increased, both significant difference (P<0.01).When given inhibitor SB203580,the expression of P38 and OX42 significantly decreased (P<0.01). The behavioral performance of IBS rats significantly decreased compared with normal rats, there is no significant difference between them (P>0.05).ConclusionThe visceral hypersensitivity in IBS can cause changes in microglia in DCN, there is a close relationship between the progam and microglia..Visceral hypersensitivity in IBS may be activated by the MAPK-P38 signal pathway of the microglia in DCN.