Masayuki Uchida1,*, Kei Matsueda2, Ryosuke Shoda2,
Akira Muraoka2 and Shigeru Yamato2
1Food Functionality Research Institute, Meiji Milk Products
Co., Ltd., 540 Naruda, Odawara 250-0862, Japan
2Division of Gastroenterology, Internal Medicine, International
Medical Center, 1-21-2 Toyama, Shinjuku-ku, Tokyo 162-0052, Japan
*Corresponding author. FAX: +81-465-36-2776
E-mail: masayuki_uchida@meiji-milk.com
Abstract: Prostaglandin (PG) and nitric oxide (NO) have been known
to inhibit the lesion formation induced by necrotic agents. However, no
clear correlation between PG and NO has been shown in the gastroprotective
action against necrotic agent-induced gastric mucosal lesions in rats. Thus,
the present study was performed to clarify this correlation. Gastric mucosal
lesions were induced by the oral administration of 0.6 M HCl in rats. 16,16-Dimethyl
PGE2 (0.3-3 mg/kg, p.o.; dim-PGE2),
sodium nitrite (0.3 and 1 mg/kg, s.c.) and sodium nitroprusside (30 and
100 mg/kg, i.v.; SNP) dose-dependently inhibited
the lesion formation. Orally administered sodium nitrite or SNP (3 mg/kg)
also significantly inhibited the lesion formation. The gastroprotective
action by dim-PGE2 was not affected by the pre-treatment with
NG-nitro- L-arginine
methylester (10 mg/kg, i.v.). The gastroprotective effect by sodium nitrite
or SNP was markedly attenuated by the pre-treatment with indomethacin (10
mg/kg, s.c.). These findings suggest that NO donating compounds inhibit
the HCl-induced mucosal lesions mainly through prostaglandin, but dim-PGE2
directly inhibits the lesions without involvement of NO in rats.
Keywords: Nitric oxide, Prostaglandin, Gastric mucosal lesion
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