LI De-tang, TU Xing, CHAI Yu-na, et al. Research on Cytokine and mRNA Expression in Entorhinal Cortex and Colon Tissue of IBS-D Model Rats[J]. Chinese journal of experimental traditional medical formulae, 2015, 21(10): 128-132.
LI De-tang, TU Xing, CHAI Yu-na, et al. Research on Cytokine and mRNA Expression in Entorhinal Cortex and Colon Tissue of IBS-D Model Rats[J]. Chinese journal of experimental traditional medical formulae, 2015, 21(10): 128-132. DOI: 10.13422/j.cnki.syfjx.2015100128.
Objective: To detect the expression levels of cytokine interleukin 1β (IL-1β)
interleukin 2 (IL-2) and tumor necrosis factor alpha (TNF-α) as well as the mRNA expression in hippocampus and colon tissues of diarrhea predominant irritable bowel syndrome (IBS-D) rat model
and to make a preliminary analysis of the pathogenesis of brain-gut axis in IBS-D. Method: Thirty Sprague Dawley rats were divided into the normal group (n=10) and the model group (n=20). The IBS-D rat model was replicated in the model group
and the expression levels of IL-1β
IL-2 and TNF-α were detected by using immunohistochemical analysis
the mRNA expressions of IL-1β
IL-2 and TNF-α were detected by using fluorescence quantitative PCR method. The relationship of the different expression in hippocampus and colon tissues was analyzed by using SPSS 13.0. Result: Compared with the normal group
the levels of IL-1β
IL-2 and TNF-α in the hippocampus and colon tissue of increased significantly in the model group
and the results showed some degree of correlation between the hippocampus and colon tissue. The mRNA expression of IL-1β in the hippocampus of IBS-D rats increased significantly
the mRNA expression of TNF-α in the hippocampus and colon tissues increased significantly(P<0.05)
but there were no significant changes in the mRNA expression level of IL-2. Conclusion: As the mediators of inflammation
the expressions of IL-1β
IL-2 and TNF-α
were abnormal in the hippocampus and colon tissues of the IBS-D rats
suggesting that the occurrence and development of IBS-D may be contributed by the effect of nerve endocrine immune network and the realization of brain-gut axis function changes.