Effects of vanilloid receptor agonists and antagonists on gastric antral ulcers in rats

Yamamoto, Hisashi; Horie, Syunji; Uchida, Masayuki; Tsuchiya, Shizuko; Murayama, Toshihiko; Watanabe, Kazuo

doi:10.1016/s0014-2999(01)01481-9

Cited by 36 publications

(22 citation statements)

References 35 publications

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“…The TRPV1 agonists were proved effective in protecting gastric mucosa against various experimentally induced ulcer models (Yamamoto et al, 2001;Horie et al, 2004). Activation of TRPV1 results in stimulation of capsaicin-sensitive afferent neurons (CSN) with the release of CGRP that increases gastric mucosal blood flow (Aihara et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of gastroprotective effect of eugenol in indomethacin‐induced ulcer in rats

Morsy

Fouad

2008

Phytotherapy Research

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Possible mechanisms underlying the gastroprotective effect of eugenol against indomethacin-induced ulcer in rats were investigated. Pyloric ligation was performed for collection of gastric juice, and gastric ulceration was induced by a single intraperitoneal (i.p.) injection of indomethacin (30 mg/kg). Pretreatment with a single dose of eugenol (100 mg/kg, orally), 1 h before indomethacin administration caused significant reductions in gastric mucosal lesions, gastric acid outputs and pepsin activity associated with a significant increase in mucin concentration. Additionally, eugenol significantly attenuated the elevations in gastric mucosal malondialdehyde and total nitrite, and the decrease in reduced glutathione observed with indomethacin. The protective effect afforded by eugenol was significantly inhibited by prior administration of glibenclamide, the ATP-sensitive potassium (K(ATP)) channel blocker, but not by prior use of ruthenium red, the transient receptor potential vanilloid 1 (TRPV1) antagonist. The results indicate that the anti-ulcer effect of eugenol is mediated by opening of K(ATP) channels, scavenging free radicals, decreasing acid-pepsin secretion, increasing mucin production, and preventing the deleterious rise in nitric oxide level.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of gastroprotective effect of eugenol in indomethacin‐induced ulcer in rats

Morsy

Fouad

2008

Phytotherapy Research

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“…Because the present study was done using only one injury model and because the mechanisms for gastric protection are different depending on the model, further study is certainly required to verify these points using other different injury models. In addition, it remains unknown whether endogenous PGs modulate the capsaicin action through interaction with VR1, although capsaicin exhibits gastric protection through activation of VR1 (Yamamoto et al, 2001). Recent studies demonstrated that endogenous posphatidylinositol-4,5-bisphosphate [PtdIns(4,5)P 2 ] inhibits VR1 and the repression can be alleviated by agents that activate phospholipase C (Premkumar and Ahern, 2000;Chuang et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Facilitation by Endogenous Prostaglandins of Capsaicin-Induced Gastric Protection in Rodents through EP2 and IP Receptors

Takeuchi¹,

Kato²,

Takeeda³

et al. 2002

J Pharmacol Exp Ther

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We investigated the role that prostaglandins (PGs) and EP receptors play in facilitating the gastroprotective action of capsaicin against HCl/ethanol in rats and mice. Male SpragueDawley rats and C57BL/6 mice were used after 18 h of fasting. The animals were given HCl/ethanol (60% in 150 mM HCl) p.o. and killed 1 h later. Capsaicin or various EP agonists were given p.o. 30 min or i.v. 10 min before HCl/ethanol. In some cases, indomethacin or various EP agonists were given s.c. 30 min or i.v 10 min before capsaicin, respectively. Gastric lesions induced by HCl/ethanol were significantly inhibited by PGE 2 as well as capsaicin. The effect of PGE 2 was antagonized by ONO-AE-829 (EP1 antagonist), whereas the capsaicin action was mitigated by indomethacin as well as sensory deafferentation but not by ONO-AE-829. The generation of mucosal PGE 2 was not affected by either capsaicin or sensory deafferentation, but was significantly inhibited by indomethacin. Although neither butaprost (EP2), ONO-NT-012 (EP3), nor 11-deoxy PGE1 (EP4) alone had any effect on HCl/ethanolinduced gastric lesions, only butaprost restored the protective action of capsaicin in the presence of indomethacin. Capsaicin provided a protective action against HCl/ethanol-induced gastric lesions in wild-type (ϩ/ϩ) mice in an indomethacin-sensitive manner, and this action was similarly observed in EP1 (Ϫ/Ϫ) and EP3 (Ϫ/Ϫ) mice but not in the animals lacking IP receptors. These results suggest that capsaicin exhibits gastric cytoprotection, essentially by stimulating sensory neurons, and this action is facilitated by endogenous PGs through EP2/IP receptors, probably sensitizing the sensory neurons to capsaicin.

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“…On the other hand, oral administration of capsaicin (20 mg / kg) prevented the NH 2 Cl-induced gastric lesions in the intact rats, but was no longer effective in sensory denervated rats. Ruthenium red is known to be a blocker of capsaicin-activated cation channels (15,16). As shown in Fig.…”

Section: Effect Of Ig On Nh 2 Cl-induced Gastric Lesionsmentioning

confidence: 99%

Irsogladine Prevents Monochloramine-Induced Gastric Mucosal Lesions by Improving the Decrease in Mucosal Blood Flow Due to the Disturbance of Nitric Oxide Synthesis in Rats

et al. 2003

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Abstract. The inhibitory effect of an anti-ulcer drug irsogladine [2,4-diamino-6-(2,5-dichlorophenyl)-s-triazine maleate] on monochloramine (NH 2 Cl)-induced gastric mucosal lesions and its mechanisms of action were clarified in rats. Irsogladine dose-dependently prevented the formation of gastric mucosal lesions induced by 60 mM NH 2 Cl. The mucosal protective effect of irsogladine was not influenced by capsaicin-sensitive sensory defunctionalization. On the other hand, its protective effect was diminished by the inhibitor of nitric oxide synthase N G -nitro-Larginine methylester (L-NAME), but not by the inducible nitric oxide synthase selective inhibitor aminoguanidine. Irsogladine restored the NH 2 Cl-induced decrease in the gastric cGMP formation as an index of nitric oxide synthesis, while it alone had no influence on the cGMP formation in intact tissues. Pretreatment with L-NAME abolished the recovery of cGMP by irsogladine. Furthermore, irsogladine ameliorated the NH 2 Cl-induced decrease in gastric mucosal blood flow, which was also reversed by pretreatment with L-NAME. These findings suggest that the improvement of the decrease in mucosal blood flow subsequent to the disturbance of gastric nitric oxide synthesis is involved in the protective effect of irsogladine on gastric mucosal lesions caused by NH 2 Cl.

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Effects of vanilloid receptor agonists and antagonists on gastric antral ulcers in rats

Cited by 36 publications

References 35 publications

Mechanisms of gastroprotective effect of eugenol in indomethacin‐induced ulcer in rats

Mechanisms of gastroprotective effect of eugenol in indomethacin‐induced ulcer in rats

Facilitation by Endogenous Prostaglandins of Capsaicin-Induced Gastric Protection in Rodents through EP2 and IP Receptors

Irsogladine Prevents Monochloramine-Induced Gastric Mucosal Lesions by Improving the Decrease in Mucosal Blood Flow Due to the Disturbance of Nitric Oxide Synthesis in Rats

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