Transient Prevention of Ethanol-Induced Gastric Lesion by Capsaicin Due to Release of Endogenous Calcitonin Gene-Related Peptide in Rats

Hayashi, Hiromi; Ohno, Takashi; Nishiyama, Kazuo; Boku, Katsuharu; Katori, Makoto; Murakami, Masataka

doi:10.1254/jjp.86.351

Cited by 15 publications

(14 citation statements)

References 13 publications

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“…CGRP is synthesized by sensory C-fibers throughout the respiratory tree and potently constricts airway smooth muscle (11). The tissues contained considerably more CGRP compared with substance P (12,13). We reported that CGRP also exhibited important roles in the gastrointestinal tract (14,15).…”

Section: Expressions Of Growth Factors In Tumor Stromal Tissues In Cgrp-mentioning

confidence: 88%

Neuronal system-dependent facilitation of tumor angiogenesis and tumor growth by calcitonin gene-related peptide

Toda

Suzuki²,

Hosono³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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118

110

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Section: Expressions Of Growth Factors In Tumor Stromal Tissues In Cgrp-mentioning

confidence: 88%

Neuronal system-dependent facilitation of tumor angiogenesis and tumor growth by calcitonin gene-related peptide

Toda

Suzuki²,

Hosono³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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118

110

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“…We previously reported that 50% ethanol caused immediate development of mucosal lesions within four minutes after contact with the mucosa. 11 Therefore, in the present experiment, we exposed the gastric mucosa for four minutes to this concentration of ethanol, which was then replaced with physiological saline containing 10 µg/ml pepstatin.…”

Section: Surgical Preparation For Stomach Perfusionmentioning

confidence: 99%

“…11 To obtain a high recovery of endogenous CGRP released into the gastric lumen, 10 µg/ml of pepstatin, a dose sufficient to inhibit pepsin released from the stomach, was added to the perfusate. Perfusates were collected into plastic tubes and kept on ice.…”

Section: Measurement Of Intragastric Cgrpmentioning

confidence: 99%

“…[6][7][8][9][10] We reported previously that capsaicin released CGRP, and prevented ethanol induced gastric mucosal injury. 11 In our series of intravital microscopic studies, [11][12][13][14] ethanol induced rat gastric mucosal injury was initially attributed to congestion of mucosal blood flow, which was caused by constriction of the collecting venules of the gastric mucosa. Both CGRP and capsaicin prevented ethanol induced constriction of the collecting venules and inhibited mucosal injury.…”

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confidence: 99%

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Endogenous prostaglandin I2 regulates the neural emergency system through release of calcitonin gene related peptide

Arai

Ohno

Saeki

et al. 2003

Gut

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Background: We previously reported that endogenous prostaglandin I 2 , generated by a mild irritant, sensitised calcitonin gene related peptide (CGRP) containing sensory nerves and facilitated the release of CGRP and gastric mucosal protection against ethanol. Administration of capsaicin also inhibited ethanol induced gastric mucosal injury through immediate release of CGRP from primary sensory neurones, which is termed the neural emergency system. In the present study, we tested whether endogenous prostaglandin I 2 also modulates the cytoprotective action of capsaicin using prostaglandin I receptor knockout mice (IP −/− ). Methods: The stomachs of IP −/− or their wild-type counterparts (IP +/+ ), anaesthetised with urethane (1.225 g/kg), were doubly cannulated from the oesophageal and duodenal sides, and the gastric mucosa was perfused (1 ml/min) with physiological saline. Perfusate was changed to 50% ethanol alone, or 50% ethanol containing capsaicin (16∼1600 µM). The injured area was estimated at the end of each perfusion experiment. In some animals, CGRP-(8-37), a CGRP antagonist (0.3 mg/kg), or indomethacin (1 mg/kg) was intravenously injected before perfusion of 50% ethanol containing capsaicin. Results: Capsaicin inhibited the injured area in a dose dependent manner. Fifty per cent ethanol containing capsaicin (480 µM) immediately increased intragastric levels of CGRP although 50% ethanol alone did not. The protective action of capsaicin (480 µM) against ethanol was completely abolished by intravenous injection of CGRP-(8-37). Indomethacin also inhibited the protective action of capsaicin, and this was accompanied by reduced levels of intragastric CGRP. Intragastric levels of prostaglandin E 2 were not increased by capsaicin treatment but those of 6-keto-prostaglandin F 1α , a metabolite of prostaglandin I 2 , were markedly increased. No protective action of capsaicin was observed in IP −/− which lacked the ability to increase intragastric CGRP levels in response to ethanol containing capsaicin. The CGRP content of the stomach from untreated IP −/− did not differ from those in IP +/+ . Capsaicin (160 µM) together with intragastric perfusion of beraprost sodium (PGI 2 analogue, 2.5 µg/ml) showed enhanced protection against ethanol induced injury. This enhanced protection was completely blocked by intravenous injection of CGRP-(8-37). Conclusions: The present results suggest that endogenous prostaglandin I 2 enhances the protective action of the capsaicin mediated neural emergency system against ethanol induced gastric mucosal injury through enhancement of CGRP release.

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“…Perfusion of the stomach with mere 50% ethanol or physiological saline + pepstatin does not increase CGRP. 330 In a study of protection by CGRP against ethanol it is observed that the i.a mode of administration but not s.c, i.v, or i.g. is effective indicating that it is close to release of the vasodilatory peptide.…”

Section: Protection By (I) Capsaicinmentioning

confidence: 99%

Capsaicin and Gastric Ulcers

2006

Critical Reviews in Food Science and Nutrition

108

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In recent years, infection of the stomach with the organism Helicobacter Pylori has been found to be the main cause of gastric ulcers, one of the common ailments afflicting humans. Excessive acid secretion in the stomach, reduction in gastric mucosal blood flow, constant intake of non-steroid anti-inflammatory drugs (NSAIDS), ethanol, smoking, stress etc. are also considered responsible for ulcer formation. The prevalent notion among sections of population in this country and perhaps in others is that "red pepper" popularly known as "Chilli," a common spice consumed in excessive amounts leads to "gastric ulcers" in view of its irritant and likely acid secreting nature. Persons with ulcers are advised either to limit or avoid its use. However, investigations carried out in recent years have revealed that chilli or its active principle "capsaicin" is not the cause for ulcer formation but a "benefactor." Capsaicin does not stimulate but inhibits acid secretion, stimulates alkali, mucus secretions and particularly gastric mucosal blood flow which help in prevention and healing of ulcers. Capsaicin acts by stimulating afferent neurons in the stomach and signals for protection against injury causing agents. Epidemiologic surveys in Singapore have shown that gastric ulcers are three times more common in the "Chinese" than among Malaysians and Indians who are in the habit of consuming more chillis. Ulcers are common among people who are in the habit of taking NSAIDS and are infected with the organism "Helicobacter Pylori," responsible for excessive acid secretion and erosion of the mucosal layer. Eradication of the bacteria by antibiotic treatment and avoiding the NSAIDS eliminates ulcers and restores normal acid secretion.

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Transient Prevention of Ethanol-Induced Gastric Lesion by Capsaicin Due to Release of Endogenous Calcitonin Gene-Related Peptide in Rats

Cited by 15 publications

References 13 publications

Neuronal system-dependent facilitation of tumor angiogenesis and tumor growth by calcitonin gene-related peptide

Neuronal system-dependent facilitation of tumor angiogenesis and tumor growth by calcitonin gene-related peptide

Endogenous prostaglandin I2 regulates the neural emergency system through release of calcitonin gene related peptide

Capsaicin and Gastric Ulcers

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