Exogenous H2S promotes ion channel reconstruction to regulate colonic motility in rats with dinitrobenzene sulfonic acid-induced colitis.

BACKGROUND

Hydrogen sulfide (H2S) is a newly recognized endogenously generated gasotransmitter. Endogenous H2S has been shown to be related to several gastrointestinal diseases, including irritable bowel syndrome, Crohn's disease, and ulcerative colitis. We explored the functional role of H2S in colitis and investigated the underlying mechanism.

METHODS

Rats were randomly divided into control, model, and sodium hydrosulfide (NaHS) groups. Rat colitis was evaluated using the disease activity index and hematoxylin and eosin (HE) staining. The collected rat feces and intestinal charcoal transit were examined to determine intestinal motility. Enzyme-linked immunoassay kits were used to determine inflammatory factors in the rat blood. Calcium ion distribution and the protein expression of Potassium voltage gated channel subfamily D member 3 (KCND3), Maxi Potassium channel alpha (KCNMA1) and potassium inwardly rectifying channel J8 (KCNJ8) in rat smooth muscle were determined using an intracellular calcium detection kit, quantitative-reverse transcription polymerase chain reaction (qRT-PCR) and Western blot, respectively.

RESULTS

The results showed that H2S donor NaHS improved the intestinal mucosa of colitis rats by alleviating the tissue edema and congestion and repairing the gland structure of the intestinal mucosa. NaHS also reduced the levels of inflammatory factors containing interleukin (IL)-1β, tumor necrosis factor alpha, and IL-6 in the rat blood. Additionally, the NaHS intervention partially restored rat intestinal motility by downregulating the proteins and mRNA expression of KCND3, KCNMA1, and KCNJ8 to reconstruct the ion channels.

CONCLUSIONS

Our findings provide novel insights into the effect of H2S regulation on the anti-inflammatory action.