Effects of electroacupuncture at Zusanli (ST 36) on neurons in the colonic myenteric plexus in rats with irritable bowel syndrome with constipation

We studied the effects of electroacupuncture at Zusanli （ST 36） on neurons in the colonic myenteric plexus and on defecation in rats with irritable bowel syndrome with constipation （IBS-C）. We also used intragastric administration of pinaverium bromide as a positive control treatment to reveal the pathway mediating the onset of IBS-C. Both electroacupuncture and pinaverium bromide greatly improved defecation in rats with IBS-C. Immunohistochemical staining of the enteric nervous system neuronal marker protein gene product 9.5 in the colonic myenteric plexus showed that electroacupuncture by itself, or in combination with pinaverium bromide, increased the number of neurons and the staining intensity of protein gene product 9.5 in the colonic myenteric plexus. We conclude that visceral hypersensitivity is likely to be a primary cause of constipation in IBS-C rats.

Involvement of nitrergic neurons in colonic motility in a rat model of ulcerative colitis

BACKGROUND The mechanisms underlying gastrointestinal(GI)dysmotility with ulcerative colitis(UC)have not been fully elucidated.The enteric nervous system(ENS)plays an essential role in the GI motility.As a vital neurotransmitter in the ENS,the gas neurotransmitter nitric oxide(NO)may impact the colonic motility.In this study,dextran sulfate sodium(DSS)-induced UC rat model was used for investigating the effects of NO by examining the effects of rate-limiting enzyme nitric oxide synthase(NOS)changes on the colonic motility as well as the role of the ENS in the colonic motility during UC.AIM To reveal the relationship between the effects of NOS expression changes in NOS-containing nitrergic neurons and the colonic motility in a rat UC model.METHODS Male rats(n=8/each group)were randomly divided into a control(CG),a UC group(EG1),a UC+thrombin derived polypeptide 508 trifluoroacetic acid(TP508TFA;an NOS agonist)group(EG2),and a UC+NG-monomethyl-L-arginine monoacetate(L-NMMA;an NOS inhibitor)group(EG3).UC was induced by administering 5.5%DSS in drinking water without any other treatment(EG1),while the EG2 and EG3 were gavaged with TP508 TFA and L-NMMA,respectively.The disease activity index(DAI)and histological assessment were recorded for each group,whereas the changes in the proportion of colonic nitrergic neurons were counted using immunofluorescence histochemical staining,Western blot,and enzyme linked immunosorbent assay,respectively.In addition,the contractile tension changes in the circular and longitudinal muscles of the rat colon were investigated in vitro using an organ bath system.RESULTS The proportion of NOS-positive neurons within the colonic myenteric plexus(MP),the relative expression of NOS,and the NOS concentration in serum and colonic tissues were significantly elevated in EG1,EG2,and EG3 compared with CG rats.In UC rats,stimulation with agonists and inhibitors led to variable degrees of increase or decrease for each indicator in the EG2 and EG3.When the rats in EGs developed UC,the mean contraction tension of the colonic smooth muscle detected in vitro was higher in the EG1,EG2,and EG3 than in the CG group.Compared with the EG1,the contraction amplitude and mean contraction tension of the circular and longitudinal muscles of the colon in the EG2 and EG3 were enhanced and attenuated,respectively.Thus,during UC,regulation of the expression of NOS within the MP improved the intestinal motility,thereby favoring the recovery of intestinal functions.CONCLUSION In UC rats,an increased number of nitrergic neurons in the colonic MP leads to the attenuation of colonic motor function.To intervene NOS activity might modulate the function of nitrergic neurons in the colonic MP and prevent colonic motor dysfunction.These results might provide clues for a novel approach to alleviate diarrhea symptoms of UC patients.