» Articles » PMID: 35095514

Effects of Exogenous Hydrogen Sulfide in the Hypothalamic Paraventricular Nucleus on Gastric Function in Rats

Overview
Journal Front Pharmacol
Date 2022 Jan 31
PMID 35095514
Authors
Affiliations
Soon will be listed here.
Abstract

Hydrogen sulfide (HS) is a new type of gas neurotransmitter discovered in recent years. It plays an important role in various physiological activities. The hypothalamus paraventricular nucleus (PVN) is an important nucleus that regulates gastric function. This study aimed to clarify the role of HS in the paraventricular nucleus of the hypothalamus on the gastric function of rats. An immunofluorescence histochemistry double-labelling technique was used to determine whether cystathionine-beta-synthase (CBS) and c-Fos neurons are involved in PVN stress. Through microinjection of different concentrations of NaHS, physiological saline (PS), D-2-Amino-5-phosphonovaleric acid (D-AP5), and pyrrolidine dithiocarbamate (PDTC), we observed gastric motility and gastric acid secretion. c-Fos and CBS co-expressed the most positive neurons after 1 h of restraint and immersion, followed by 3 h, and the least was at 0 h. After injection of different concentrations of NaHS into the PVN, gastric motility and gastric acid secretion in rats were significantly inhibited and promoted, respectively ( < 0.01); however, injection of normal saline, D-AP5, and PDTC did not cause any significant change ( > 0.05). The suppressive effect of NaHS on gastrointestinal motility and the promotional effect of NaHS on gastric acid secretion could be prevented by D-AP5, a specific N-methyl-D-aspartic acid (NMDA) receptor antagonist, and PDTC, an NF-B inhibitor. There are neurons co-expressing CBS and c-Fos in the PVN, and the injection of NaHS into the PVN can inhibit gastric motility and promote gastric acid secretion in rats. This effect may be mediated by NMDA receptors and the NF-B signalling pathway.

Citing Articles

Hydrogen Sulfide (HS) Generated in the Colon Induces Neuropathic Pain by Activating Spinal NMDA Receptors in a Rodent Model of Chronic Constriction Injury.

Wang J, Zhang N, Liu H, Wang J, Zhang Y, Su D Neurochem Res. 2025; 50(2):90.

PMID: 39883291 DOI: 10.1007/s11064-025-04342-w.


Analysis of microRNAs and the microRNA-messengerRNA regulatory network in chronic alcohol exposure.

Du A, Chen Y, Qiao S, Dong J, Li Y, Cao B Front Pharmacol. 2024; 15:1377501.

PMID: 39234114 PMC: 11371712. DOI: 10.3389/fphar.2024.1377501.


Investigating the L-Glu-NMDA receptor-HS-NMDA receptor pathway that regulates gastric function in rats' nucleus ambiguus.

Sun H, Li C, Shi Y, Wang Y, Li J, Fan L Front Pharmacol. 2024; 15:1389873.

PMID: 38751777 PMC: 11094298. DOI: 10.3389/fphar.2024.1389873.


Effect of exogenous hydrogen sulfide in the nucleus tractus solitarius on gastric motility in rats.

Sun H, Li C, Shi Y, Li J, Wang Y, Han L World J Gastroenterol. 2023; 29(29):4557-4570.

PMID: 37621756 PMC: 10445002. DOI: 10.3748/wjg.v29.i29.4557.

References
1.
Sen N, Paul B, Gadalla M, Mustafa A, Sen T, Xu R . Hydrogen sulfide-linked sulfhydration of NF-κB mediates its antiapoptotic actions. Mol Cell. 2012; 45(1):13-24. PMC: 3261430. DOI: 10.1016/j.molcel.2011.10.021. View

2.
Hu L, Lu M, Wong P, Bian J . Hydrogen sulfide: neurophysiology and neuropathology. Antioxid Redox Signal. 2010; 15(2):405-19. DOI: 10.1089/ars.2010.3517. View

3.
Chen X, Liu X . Hydrogen sulfide from a NaHS source attenuates dextran sulfate sodium (DSS)-induced inflammation via inhibiting nuclear factor-κB. J Zhejiang Univ Sci B. 2016; 17(3):209-17. PMC: 4794512. DOI: 10.1631/jzus.B1500248. View

4.
Glowacka U, Brzozowski T, Magierowski M . Synergisms, Discrepancies and Interactions between Hydrogen Sulfide and Carbon Monoxide in the Gastrointestinal and Digestive System Physiology, Pathophysiology and Pharmacology. Biomolecules. 2020; 10(3). PMC: 7175135. DOI: 10.3390/biom10030445. View

5.
Collin M, Anuar F, Murch O, Bhatia M, Moore P, Thiemermann C . Inhibition of endogenous hydrogen sulfide formation reduces the organ injury caused by endotoxemia. Br J Pharmacol. 2005; 146(4):498-505. PMC: 1751176. DOI: 10.1038/sj.bjp.0706367. View