Preliminary Comparative Study On The Visceral Sensitivity Mechanism Of Irritable Bowel Syndrome And Ulcerative Colitis In Remission In Rats

Background and Objective:Ulcerative colitis(UC)is a chronic inflammatory disease of the gastrointestinal tract with unknown etiology.Nearly half of patients with UC in remission(UCR)have abdominal pain,abdominal discomfort,which are more common in irritable bowel syndrome(IBS).The mechanism is still unclear,which poses great difficulties for clinical diagnosis and treatment.The pathogenesis of IBS involves visceral hypersensitivity,mucosal inflammation and immune abnormalities,intestinal dysmotility,etc.In this study,we established rat models of UCR and IBS,centered on visceral hypersensitivity,and compared UCR and IBS in peripheral enteric nerves and mast cells,and initially explored the similarities and differences between UCR and IBS in pathophysiological mechanisms.Materials and Methods:IBS rat model was established by combining slow and acute stress.Dextran sulfate sodium(DSS)feeding was used to establish UC rat models in active and remissive period.Body weight,12-hour stool volume and water content,rectal globule discharge time,abdominal wall reflex reflex(AWR)score and pain threshold,histological inflammation were evaluated.The distal colon specimens were taken and the number of anti-HuC/D-immunoreactivity(IR)positive neurons,mast cells(MC)and nerve growth factor(NGF)-IR positive cells in the colon of each group were observed by immunofluorescence staining.Quantitative analysis was performed using Image Pro Plus software.Results:7 IBS rats,5 active UC(AUC)rats,8 UC in remission(UCR)rats,and 8 healthy control(HC)rats finished the experiment.?The weight gain of rats in AUC group was significantly slower than that in HC(414.80±31.83g vs 490.25±58.15g,P<0.05),IBS(451.75±34.40g)and UCR group(451.75±34.40g)had no significant differences compared with the HC group.?During the modeling period,the number of fecal pellets and water content in the AUC,UCR,and IBS groups increased,which was significantly higher than that in the HC group.There was no significant difference in the fecal traits among the UCR,IBS and HC group.?The rectal globule discharge time of the UCR group was significantly shorter than that of the IBS and HC group(5.83±1.73min vs 18.30±13.11min and 21.40±10.33min,respectively,P<0.05);?The AWR scores of rats in IBS group were significantly higher than those in HC and UCR group at pressure level of 20mmHg and 40mmHg(P<0.05).The pain threshold in IBS group was significantly lower than that in UCR group(41.43±9.0mmHg vs 67.50±10.35mmHg,P<0.05);?Compared with AUC group,inflammatory cell infiltration and ulcer were less in UCR group,which showed the connective tissue regeneration in the ulcer and lymphocytic infiltration mainly and chronic inflammation changes such as crypt branching.There was no significant difference between the IBS and HC group;?The number of intestinal mast cells in UCR and IBS group was significantly higher than that in HC group[15.0(7.0),11.0(5.0)vs 8.0(6.0),P<0.05],and the UCR group was significantly more than IBS(P<0.05).The proportion of activated mast cells in UCR and IBS group was higher than that in HC group(P>0.05).The number of NGF-IR positive cells in UCR and IBS-D group was significantly higher than that in HC group[11.0(8.0)6.0(3.0)vs 4.0(5.0),P<0.05],and the UCR group was significantly more than IBS group(P<0.05).Some MCs were NGF-IR positive;?The numbers of enteric neurons in IBS,UCR groups were lower than that in the HC group(40.0±10.95,46.54±8.44 vs 55.10±10.4,P<0.05),and neurons in UCR group were more than that in IBS group(P>0.05).Conclusions:?IBS rat model can be built by combining chronic and acute stress.The intestinal tissue of UCR rats showed chronic inflammation,and there were abnormal intestinal motility,and visceral hypersensitivity was not obvious.?IBS,AUC and UCR rats had different degrees of intestinal neurons reduction.Neuronal injury can relieve with short-term inflammation improvement;?Visceral sensitivity of IBS and UCR rats changed in different degrees,which are related to MCs and their activation,and the expression of NGF,but there may be different in other inflammatory mediators,peripheral intestinal neurotransmitters,central pain management,etc;?There may be some commonality in the pathogenesis of IBS and UCR,in which the inflammatory response may play a greater role in the UCR.