Lactobacillus reuteri DSM 17938 Protects against Gastric Damage Induced by Ethanol Administration in Mice: Role of TRPV1/Substance P Axis

This study aimed to evaluate the effect of Lactobacillus reuteri DSM 17938 (DSM) on ethanol-induced gastric injury, and if its possible mechanism of action is related to inhibiting the transient receptor potential vanilloid type 1 (TRPV1). We evaluated the effect of supplementing 108 CFU•g body wt−1•day−1 of DSM on ethanol-induced gastric injury. DSM significantly reduced the ulcer area (1.940 ± 1.121 mm2) with 3 days of pretreatment. The effects of DSM supplementation were reversed by Resiniferatoxin (RTX), TRPV1 agonist (3 nmol/kg p.o.). Substance P (SP) (1 μmol/L per 20 g) plus 50% ethanol resulted in hemorrhagic lesions, and DSM supplementation did not reverse the lesion area induced by administering SP. TRPV1 staining intensity was lower, SP, malondialdehyde (MDA) and nitrite levels were reduced, and restored normal levels of antioxidant parameters (glutathione and superoxide dismutase) in the gastric mucosa in mice treated with DSM. In conclusion, DSM exhibited gastroprotective activity through decreased expression of TRPV1 receptor and decreasing SP levels, with a consequent reduction of oxidative stress.

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Transient receptor potential vanilloid 1 and transient receptor potential ankyrin 1 contribute to the progression of colonic inflammation in dextran sulfate sodium-induced colitis in mice: Links to calcitonin gene-related peptide and substance P

Journal of Pharmacological Sciences ◽

10.1016/j.jphs.2017.12.012 ◽

2018 ◽

Vol 136 (3) ◽

pp. 121-132 ◽

Cited By ~ 16

Author(s):

Daichi Utsumi ◽

Kenjiro Matsumoto ◽

Takuya Tsukahara ◽

Kikuko Amagase ◽

Makoto Tominaga ◽

...

Keyword(s):

Substance P ◽

Transient Receptor Potential ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Receptor Potential ◽

Transient Receptor Potential Vanilloid ◽

Colonic Inflammation ◽

Related Peptide ◽

Calcitonin Gene ◽

Transient Receptor

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Substance P, proinflammatory cytokines, transient receptor potential vanilloid subtype 1 and COVID-19: a working hypothesis

Neurología (English Edition) ◽

10.1016/j.nrleng.2020.10.002 ◽

2021 ◽

Vol 36 (2) ◽

pp. 184-185

Author(s):

E.E. Aguirre-Siancas ◽

E. Colona-Vallejos ◽

E. Ruiz-Ramirez ◽

M. Becerra-Bravo ◽

L. Alzamora-Gonzales

Keyword(s):

Substance P ◽

Proinflammatory Cytokines ◽

Transient Receptor Potential ◽

Receptor Potential ◽

Transient Receptor Potential Vanilloid ◽

Working Hypothesis ◽

Transient Receptor

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Analysis of transient receptor potential vanilloid 1 and substance P gene expression in the mouse tongue following oral ginger administration

The Journal of Phytopharmacology ◽

10.31254/phyto.2016.5401 ◽

2016 ◽

Vol 5 (4) ◽

pp. 131-134

Author(s):

Iizuka Michiro ◽

◽

Hirata Ayumu ◽

Abe Noriaki ◽

Jobu Kohei ◽

...

Keyword(s):

Gene Expression ◽

Substance P ◽

Protein Expression ◽

Mrna Expression ◽

Transient Receptor Potential ◽

Receptor Potential ◽

Transient Receptor Potential Vanilloid ◽

P Gene ◽

Glandular Cells ◽

Transient Receptor

Ginger rhizome (Zingiber officinale) exhibits multiple pharmacological actions. For example, its pungent components target the transient receptor potential vanilloid 1 (TRPV1) ion channel and thus contribute to swallowing reflex recovery by elevating the neuropeptide substance P. However, the precise mechanism underlying this action remains unclear. To examine TRPV1 and substance P gene expression in the mouse tongue in response to stimulation by orally administered ginger, quantitative real-time polymerase chain reaction and immunohistochemistry were performed to evaluate mRNA and protein expression. TRPV1 mRNA expression in the mouse tongue was upregulated 30 min after oral ginger stimulation. In the gingerstimulated mouse, TRPV1 protein expression was increased and concentrated in the plasma membranes of the mucous glandular cells of the tongue epithelium. No significant differences in substance P mRNA expression relative to the control were observed after ginger stimulation. However, immunohistochemistry revealed that the amount of substance P protein expression increased in the mucous glandular cells of the tongue epithelium in ginger-stimulated mice, and this expression appeared to concentrate in the secretory granules of these cells. Activation of TRPV1 promotes the secretion of substance P in saliva, and clinically, saliva levels of substance P can be measured noninvasively and can provide a useful biomarker of the swallowing function. An increased level of substance P in the saliva could indicate improved dysphagia. Our data suggest that ginger activates TRPV1 and promotes the secretion of substance P in saliva. Ginger is therefore expected to serve as a functional agent for improving dysphagia.

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Cardioprotection by ischemic postconditioning is lost in isolated perfused heart from diabetic rats: Involvement of transient receptor potential vanilloid 1, calcitonin gene-related peptide and substance P

Regulatory Peptides ◽

10.1016/j.regpep.2011.04.004 ◽

2011 ◽

Vol 169 (1-3) ◽

pp. 49-57 ◽

Cited By ~ 34

Author(s):

Jing-Yi Ren ◽

Jun-Xian Song ◽

Ming-Yu Lu ◽

Hong Chen

Keyword(s):

Substance P ◽

Transient Receptor Potential ◽

Receptor Potential ◽

Diabetic Rats ◽

Ischemic Postconditioning ◽

Transient Receptor Potential Vanilloid ◽

Isolated Perfused Heart ◽

Perfused Heart ◽

Calcitonin Gene ◽

Transient Receptor

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Transient receptor potential vanilloid 1, calcitonin gene-related peptide, and substance P mediate nociception in acute pancreatitis

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00154.2005 ◽

2006 ◽

Vol 290 (5) ◽

pp. G959-G969 ◽

Cited By ~ 57

Author(s):

Elizabeth C. Wick ◽

Steven G. Hoge ◽

Sarah W. Grahn ◽

Edward Kim ◽

Lorna A. Divino ◽

...

Keyword(s):

Substance P ◽

Dorsal Horn ◽

Transient Receptor Potential ◽

Necrotizing Pancreatitis ◽

Receptor Potential ◽

Sensory Nerves ◽

Transient Receptor Potential Vanilloid ◽

Spinal Neurons ◽

Fos Expression ◽

Transient Receptor

The mechanism of pancreatitis-induced pain is unknown. In other tissues, inflammation activates transient receptor potential vanilloid 1 (TRPV1) on sensory nerves to liberate CGRP and substance P (SP) in peripheral tissues and the dorsal horn to cause neurogenic inflammation and pain, respectively. We evaluated the contribution of TRPV1, CGRP, and SP to pancreatic pain in rats. TRPV1, CGRP, and SP were coexpressed in nerve fibers of the pancreas. Injection of the TRPV1 agonist capsaicin into the pancreatic duct induced endocytosis of the neurokinin 1 receptor in spinal neurons in the dorsal horn (T10), indicative of SP release upon stimulation of pancreatic sensory nerves. Induction of necrotizing pancreatitis by treatment with l-arginine caused a 12-fold increase in the number of spinal neurons expressing the proto-oncogene c-fos in laminae I and II of L1, suggesting activation of nociceptive pathways. l-Arginine also caused a threefold increase in spontaneous abdominal contractions detected by electromyography, suggestive of referred pain. Systemic administration of the TRPV1 antagonist capsazepine inhibited c-fos expression by 2.5-fold and abdominal contractions by 4-fold. Intrathecal, but not systemic, administration of antagonists of CGRP (CGRP8–37) and SP (SR140333) receptors attenuated c-fos expression in spinal neurons by twofold. Thus necrotizing pancreatitis activates TRPV1 on pancreatic sensory nerves to release SP and CGRP in the dorsal horn, resulting in nociception. Antagonism of TRPV1, SP, and CGRP receptors may suppress pancreatitis pain.

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Transient receptor potential vanilloid type 1 channels act as mechanoreceptors and cause substance P release and sensory activation in rat kidneys

AJP Renal Physiology ◽

10.1152/ajprenal.00308.2007 ◽

2008 ◽

Vol 294 (2) ◽

pp. F316-F325 ◽

Cited By ~ 42

Author(s):

Nan-Hsiung Feng ◽

Hsang-Hsing Lee ◽

Jeng-Chaun Shiang ◽

Ming-Chieh Ma

Keyword(s):

Substance P ◽

Renal Pelvis ◽

Transient Receptor Potential ◽

Receptor Potential ◽

Receptor Activation ◽

Nerve Fibers ◽

Transient Receptor Potential Vanilloid ◽

Transient Receptor ◽

Sensory Activation

Stimulation of capsaicin receptors results in an increase in afferent renal nerve activity (ARNA), but it is unclear how capsaicin contributes to sensory activation intrarenally. Here, we studied the relationships between capsaicin receptor activation, substance P (SP) release, and the sensory response in the rat renal pelvis. Immunoblots showed that one of the capsaicin receptors, transient receptor potential vanilloid type 1 channel (TRPV1), was found in various renal tissues and was especially abundant in the renal pelvis, where most sensory nerve fibers originate. Interestingly, immunolabeling showed colocalization of TRPV1, SP, and the panneuronal marker PGP9.5 in the renal pelvis. Electrophysiological recordings showed that SP and capsaicin activated the same mechanosensitive ARNA in a single-unit preparation. Intrapelvic administration of capsaicin or a specific TRPV1 agonist, resiniferatoxin, resulted in a dose-dependent increase in multi-unit ARNA and SP release, and these effects were blocked by the TRVP1 blocker capsazepine. Inhibition of the SP receptor by L-703,606 largely prevented capsaicin- or resiniferatoxin-induced ARNA. Capsazepine also prevented intrapelvic pressure (IPP)-dependent ARNA activation and contralateral diuresis/natriuresis in the renorenal reflex at an IPP of 20 mmHg, but had no effect at an IPP of 50 mmHg. These data indicate that TRPV1, a low-pressure baroreceptor, is present in the renal pelvis and exclusively regulates neuropeptide release from primary renal afferent C-fibers in response to mechanostimulation.

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