scholarly journals Hydrogen sulfide-induced itch requires activation of Cav3.2 T-type calcium channel in mice

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Xue-Long Wang ◽  
Bin Tian ◽  
Ya Huang ◽  
Xiao-Yan Peng ◽  
Li-Hua Chen ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Hydrogen Sulfide ◽  
Calcium Channel ◽  
Intradermal Injection ◽  
Independent Manner ◽  
C Fibers ◽  
Itch Sensation ◽  
Μ Opioid Receptor ◽  
Pharmacological Blockade ◽  
Endogenous Precursor

Abstract The contributions of gasotransmitters to itch sensation are largely unknown. In this study, we aimed to investigate the roles of hydrogen sulfide (H2S), a ubiquitous gasotransmitter, in itch signaling. We found that intradermal injection of H2S donors NaHS or Na2S, but not GYY4137 (a slow-releasing H2S donor), dose-dependently induced scratching behavior in a μ-opioid receptor-dependent and histamine-independent manner in mice. Interestingly, NaHS induced itch via unique mechanisms that involved capsaicin-insensitive A-fibers, but not TRPV1-expressing C-fibers that are traditionally considered for mediating itch, revealed by depletion of TRPV1-expressing C-fibers by systemic resiniferatoxin treatment. Moreover, local application of capsaizapine (TRPV1 blocker) or HC-030031 (TRPA1 blocker) had no effects on NaHS-evoked scratching. Strikingly, pharmacological blockade and silencing of Cav3.2 T-type calcium channel by mibefradil, ascorbic acid, zinc chloride or Cav3.2 siRNA dramatically decreased NaHS-evoked scratching. NaHS induced robust alloknesis (touch-evoked itch), which was inhibited by T-type calcium channels blocker mibefradil. Compound 48/80-induced itch was enhanced by an endogenous precursor of H2S (L-cysteine) but attenuated by inhibitors of H2S-producing enzymes cystathionine γ-lyase and cystathionine β-synthase. These results indicated that H2S, as a novel nonhistaminergic itch mediator, may activates Cav3.2 T-type calcium channel, probably located at A-fibers, to induce scratching and alloknesis in mice.

scholarly journals Modulation of EndMT by Hydrogen Sulfide in the Prevention of Cardiovascular Fibrosis

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 910
Author(s):  
Lara Testai ◽  
Vincenzo Brancaleone ◽  
Lorenzo Flori ◽  
Rosangela Montanaro ◽  
Vincenzo Calderone
Keyword(s):  
Hydrogen Sulfide ◽  
Type I Collagen ◽  
Transforming Growth Factor ◽  
Smooth Muscle Actin ◽  
Type I ◽  
Vascular Endothelial ◽  
Independent Manner ◽  
Mesenchymal Transition ◽  
Adult Age ◽  
Cardiovascular Fibrosis

Endothelial mesenchymal transition (EndMT) has been described as a fundamental process during embryogenesis; however, it can occur also in adult age, underlying pathological events, including fibrosis. Indeed, during EndMT, the endothelial cells lose their specific markers, such as vascular endothelial cadherin (VE-cadherin), and acquire a mesenchymal phenotype, expressing specific products, such as α-smooth muscle actin (α-SMA) and type I collagen; moreover, the integrity of the endothelium is disrupted, and cells show a migratory, invasive and proliferative phenotype. Several stimuli can trigger this transition, but transforming growth factor (TGF-β1) is considered the most relevant. EndMT can proceed in a canonical smad-dependent or non-canonical smad-independent manner and ultimately regulate gene expression of pro-fibrotic machinery. These events lead to endothelial dysfunction and atherosclerosis at the vascular level as well as myocardial hypertrophy and fibrosis. Indeed, EndMT is the mechanism which promotes the progression of cardiovascular disorders following hypertension, diabetes, heart failure and also ageing. In this scenario, hydrogen sulfide (H2S) has been widely described for its preventive properties, but its role in EndMT is poorly investigated. This review is focused on the evaluation of the putative role of H2S in the EndMT process.

Reflex bronchial vasodilation in dogs evoked by injection of a small volume of water into a bronchus

1993 ◽  
Vol 75 (5) ◽  
pp. 2195-2202 ◽  
Author(s):  
T. E. Pisarri ◽  
H. M. Coleridge ◽  
J. C. Coleridge
Keyword(s):  
Blood Flow ◽  
Mucosal Blood Flow ◽  
Vagus Nerves ◽  
C Fibers ◽  
Autonomic Pathways ◽  
Lobar Bronchus ◽  
Anesthetized Dogs ◽  
Pharmacological Blockade ◽  
Airway Defense ◽  
Response To Water

Injection of water into a lobar bronchus stimulates airway C-fibers and rapidly adapting receptors and evokes airway defense reflexes. To determine whether this stimulus also evokes a reflex increase in bronchial blood flow (Qbr), we injected 1–2 ml of water into a lobar bronchus in anesthetized dogs. Injection decreased arterial pressure but increased Qbr from 9 +/- 1 to 21 +/- 3 ml/min. The increase had a latency of 6–8 s and reached a peak after approximately 20 s; Qbr returned to control after 60–90 s. Airway mucosal blood flow, measured by colored microspheres, increased in proportion to Qbr. In contrast, flow in an adjacent intercostal artery that did not supply the airway decreased slightly. Injection of isosmotic saline had little effect. In 13 of 16 dogs, the water-induced increase in Qbr was abolished by cutting or cooling the cervical vagus nerves and hence was entirely dependent on centrally mediated vagal pathways. When the vagus nerves were intact, about one-third of the vasodilator response remained after pharmacological blockade of muscarinic and adrenergic receptors. We conclude that in dogs the defense response to water in the lower airways includes a large increase in Qbr that is partly due to activation of nonadrenergic noncholinergic autonomic pathways.

Identification of ica-dependent biofilm production by Staphylococcus aureus clinical isolates and antibiofilm effects of ascorbic acid against biofilm production

2020 ◽  
Vol 73 (5) ◽  
pp. 261-266
Author(s):  
Sahra Kırmusaoğlu ◽  
Havva Kaşıkçı
Keyword(s):  
Staphylococcus Aureus ◽  
Ascorbic Acid ◽  
Biofilm Formation ◽  
Surface Proteins ◽  
Clinical Isolates ◽  
High Morbidity ◽  
Dependent Manner ◽  
Independent Manner ◽  
Biofilm Production ◽  
Life Threatening

AimsStaphylococcus aureus (S. aureus) is a life-threatening pathogen with high morbidity and mortality rates which causes nosocomial and community-acquired infections. Biofilm, considered to be a common virulence factor for pathogens, plays a significant role in recurrent and untreatable infections. Biofilm formation of S. aureus is mediated by synthesis of either poly-N-acetylglucosamine in an ica-dependent manner or surface proteins in an ica-independent manner. In some cases treatment is impossible and recurrent. In this study, ica-dependent biofilm-producing S. aureus isolates were detected and the anti-biofilm effect of ascorbic acid against biofilm formation of isolates was investigated.MethodsA total of 21 methicillin-sensitive S. aureus (MSSA) clinical isolates stored in our bacterial stock were used to detect ica-dependent biofilm-producing MSSA isolates. The anti-biofilm study was undertaken with three ica-dependent biofilm-producing isolates (MSSA2–4) and ATCC 29213 (MSSA1). Biofilms and the anti-biofilm effect of ascorbic acid were detected using the microtitre plate (MtP) method. 16S-rRNA, nuc, icaA and icaD genes and expression levels of icaA and icaD of isolates were detected by RT-PCR.ResultsThe minimum inhibitory concentrations (MICs) of ascorbic acid prevented biofilm formation of MSSA1 and MSSA3. Also, 1/2 MIC of ascorbic acid prevented biofilm formation of MSSA3. It was observed that biofilm formation decreased with increased concentration. There was no significant increase in ica gene expression of MSSA1 and MSSA2. Expression of icaA and icaD of MSSA3 decreased 13% and 38%, respectively. Expression of icaA in MSSA4 decreased 12%.ConclusionThe results of our study show that ascorbic acid can be used as an anti-biofilm agent to prevent biofilm formation of S. aureus and thus biofilm-related infections.

scholarly journals Unearthing The Alleviatory Mechanisms of Hydrogen Sulfide in Aluminum Toxicity in Rice

2021 ◽  
Author(s):  
Chun Quan Zhu ◽  
Wen Jun Hu ◽  
QianQian Wei ◽  
Hui Zhang ◽  
Xiao Chuang Cao ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Cell Wall ◽  
Ascorbic Acid ◽  
Hydrogen Sulfide ◽  
Aluminum Toxicity ◽  
Al Toxicity ◽  
Negative Effects ◽  
Al Content ◽  
Rice Roots ◽  
Wall Components

Abstract Hydrogen sulfide (H2S) improves aluminum (Al) resistance in rice; however, the underlying molecular mechanism remains unclear. In the present study, treatment with 30-μM Al significantly inhibited rice root growth and increased the total Al content and apoplastic and cytoplasm Al concentration in the rice roots. However, pretreatment with NaHS (H2S donor) reversed these negative effects. Transcriptomics and physiological experiments confirmed that H2S increased the ATP, sucrose, glutathione, and ascorbic acid contents, which was accompanied by decreased O2·- and H2O2 contents, to alleviate Al toxicity. H2S significantly inhibited ethylene emissions in the rice and then inhibited pectin synthesis and increased the pectin methylation degree to reduce cell wall Al deposition. The phytohormones indole-3-acetic and brassinolide were also involved in the alleviation of Al toxicity by H2S. In addition, other pathways of material and energy metabolism, secondary metabolism, cell wall components, signal transduction, and transcriptional and translational pathways in the rice roots were also regulated by H2S under Al toxicity conditions. These findings improve our understanding of how H2S affects rice responses to Al toxicity, which will facilitate further studies on crop safety.

P43 Ascorbic acid deficiency augments hyperalgesia induced by hydrogen sulfide in mice

Nitric Oxide ◽  
2014 ◽  
Vol 39 ◽  
pp. S29
Author(s):  
Maho Tsubota ◽  
Kenta Uebo ◽  
Koki Miki ◽  
Fumiko Sekiguchi ◽  
Yoshitaka Kondo ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Hydrogen Sulfide ◽  
Ascorbic Acid Deficiency ◽  
Acid Deficiency

Chemosensitivity and sensitization of nociceptive afferents that innervate the hairy skin of monkey

1993 ◽  
Vol 69 (4) ◽  
pp. 1071-1081 ◽  
Author(s):  
K. D. Davis ◽  
R. A. Meyer ◽  
J. N. Campbell
Keyword(s):  
Inflammatory Mediators ◽  
Intradermal Injection ◽  
Similar Proportion ◽  
Chemical Stimulus ◽  
Mechanical Stimuli ◽  
Chemical Mixture ◽  
C Fibers ◽  
Hairy Skin ◽  
C Fiber ◽  
Nociceptive Afferents

1. A large proportion of the cutaneous nociceptor population in monkey either does not respond to mechanical stimuli or has very high mechanical thresholds (> 6 bar). The goal of this study was to determine whether these mechanically insensitive nociceptive afferents (MIAs) differ from mechanically sensitive nociceptive afferents (MSAs) with regard to responses to chemical stimuli. 2. Teased-fiber techniques were used to record from 28 A delta-fiber (16 MIAs and 12 MSAs) and 23 C-fiber (10 MIAs and 13 MSAs) nociceptors in hairy skin of pentobarbital sodium-anesthetized monkeys. An electrocutaneous search technique was used to locate the putative receptive fields of the MIAs. The response to mechanical and heat stimuli was determined before and after intradermal injection of a standard mixture of algesic/inflammatory mediators (bradykinin, histamine, serotonin, and prostaglandin E1). 3. All 25 MSAs, but only 65% of the MIAs, responded to the chemical stimulus. The A delta-fibers, both MSAs and responsive MIAs, and the responsive C-fiber MIAs gave a robust discharge. In contrast, the C-fiber MSAs (the conventional polymodal C-fiber nociceptors) exhibited a significantly weaker response. Three MIAs responded only to the chemical mixture and not to mechanical or heat stimuli. 4. Before injection of the chemical mixture, a significantly smaller proportion of C-fiber MIAs (50%) than of C-fiber MSAs (92%) responded to heat stimuli, whereas a similar proportion (38%) of A delta-fiber MIAs and MSAs were heat sensitive. 5. Approximately one-half of the MIAs and MSAs were sensitized to mechanical stimuli after the chemical injection, as manifest by a decreased threshold and/or an enlarged receptive field. 6. The chemical injection sensitized 90% of A delta-fiber MSAs, but only 8% of A delta-fiber MIAs, to heat stimuli. In contrast, 38% of C-fibers were sensitized. 7. In 14 fibers, the chemical stimulus resulted in sensitization to mechanical stimuli without sensitization to heat stimuli, or vice versa. This dissociated sensitized state suggests that the molecular mechanisms of sensitization to heat and mechanical stimuli differ. 8. In conclusion, a large proportion of primate cutaneous nociceptors respond to intradermal injection of algesic/inflammatory mediators and may also become sensitized to mechanical and/or heat stimuli.

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