ArticleAnnals of translational medicine2022
Exogenous H2S promotes ion channel reconstruction to regulate colonic motility in rats with dinitrobenzene sulfonic acid-induced colitis.
Article in Annals of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- pH-responsive Oral liposomal delivery of hydrogen sulfide donor GYY4137 enables colon-targeted therapy for inflammatory bowel disease.Journal of nanobiotechnology · 2025Article
- Microbiota of the gastrointestinal tract: Friend or foe?World journal of gastroenterology · 2023Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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Abstract
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.
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