Exogenous H2S promotes ion channel reconstruction to regulate colonic motility in rats with dinitrobenzene sulfonic acid-induced colitis.
Hydrogen sulfide (H2S)
colitis
intestinal motility
ion channel
rats
Journal
Annals of translational medicine
ISSN: 2305-5839
Titre abrégé: Ann Transl Med
Pays: China
ID NLM: 101617978
Informations de publication
Date de publication:
Jun 2022
Jun 2022
Historique:
received:
29
03
2022
accepted:
16
06
2022
entrez:
18
7
2022
pubmed:
19
7
2022
medline:
19
7
2022
Statut:
ppublish
Résumé
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. 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. 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. Our findings provide novel insights into the effect of H2S regulation on the anti-inflammatory action.
Sections du résumé
Background
UNASSIGNED
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
UNASSIGNED
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
UNASSIGNED
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
UNASSIGNED
Our findings provide novel insights into the effect of H2S regulation on the anti-inflammatory action.
Identifiants
pubmed: 35845545
doi: 10.21037/atm-22-2126
pii: atm-10-12-681
pmc: PMC9279822
doi:
Types de publication
Journal Article
Langues
eng
Pagination
681Informations de copyright
2022 Annals of Translational Medicine. All rights reserved.
Déclaration de conflit d'intérêts
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://atm.amegroups.com/article/view/10.21037/atm-22-2126/coif). The authors have no conflicts of interest to declare.
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