ArticleMolecular pain2010
Hydrogen sulphide induces micro opioid receptor-dependent analgesia in a rodent model of visceral pain.
Article in Molecular pain, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 42 citations in OpenAlex.
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- Biological Effects of Thermal Water-Associated Hydrogen Sulfide on Human Airways and Associated Immune Cells: Implications for Respiratory Diseases.Frontiers in public health · 2019Review
- High glucose stimulates cell proliferation and Collagen IV production in rat mesangial cells through inhibiting AMPK-KInternational urology and nephrology · 2017Article
- Hydrogen Sulfide: A Worthwhile Tool in the Design of New Multitarget Drugs.Frontiers in chemistry · 2017Article
- Gut microbiota role in irritable bowel syndrome: New therapeutic strategies.World journal of gastroenterology · 2016Review
- Reverse Regulatory Pathway (H2S / PGE2 / MMP) in Human Aortic Aneurysm and Saphenous Vein Varicosity.PloS one · 2016Article
- Hydrogen sulfide-induced itch requires activation of Cav3.2 T-type calcium channel in mice.Scientific reports · 2015Article
- NOSH-aspirin (NBS-1120), a dual nitric oxide and hydrogen sulfide-releasing hybrid, reduces inflammatory pain.Pharmacology research & perspectives · 2015Article
- Epigenetic modification of DRG neuronal gene expression subsequent to nerve injury: etiological contribution to complex regional pain syndromes (Part I).Medical science monitor : international medical journal of experimental and clinical research · 2014Review
- Probiotics VSL#3 protect against development of visceral pain in murine model of irritable bowel syndrome.PloS one · 2013Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHydrogen sulphide (H2S) is a gaseous neuro-mediator that exerts analgesic effects in rodent models of visceral pain by activating KATP channels. A body of evidence support the notion that KATP channels interact with endogenous opioids. Whether H2S-induced analgesia involves opioid receptors is unknown.
methodsThe perception of painful sensation induced by colorectal distension (CRD) in conscious rats was measured by assessing the abdominal withdrawal reflex. The contribution of opioid receptors to H2S-induced analgesia was investigated by administering rats with selective mu, kappa and delta opioid receptor antagonists and antisenses. To investigate whether H2S causes mu opioid receptor (MOR) transactivation, the neuronal like cells SKNMCs were challenged with H2S in the presence of MOR agonist (DAMGO) or antagonist (CTAP). MOR activation and phosphorylation, its association to beta arrestin and internalization were measured.
resultsH2S exerted a potent analgesic effects on CRD-induced pain. H2S-induced analgesia required the activation of the opioid system. By pharmacological and molecular analyses, a robust inhibition of H2S-induced analgesia was observed in response to central administration of CTAP and MOR antisense, while kappa and delta receptors were less involved. H2S caused MOR transactivation and internalization in SKNMCs by a mechanism that required AKT phosphorylation. MOR transactivation was inhibited by LY294002, a PI3K inhibitor, and glibenclamide, a KATP channels blocker.
conclusionsThis study provides pharmacological and molecular evidence that antinociception exerted by H2S in a rodent model of visceral pain is modulated by the transactivation of MOR. This observation provides support for development of new pharmacological approaches to visceral pain.
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