The Role of Prostaglandin D₂ in the Genesis of Indomethacin-Induced Gastric Lesions in Rats

H. Goto Departments of Internal Medicine, and Biomedical Chemistry, Faculty of Medicine, University of Nagoya, Nagoya, Japan

S. Nakazawa Departments of Internal Medicine, and Biomedical Chemistry, Faculty of Medicine, University of Nagoya, Nagoya, Japan

K. Segawa Departments of Internal Medicine, and Biomedical Chemistry, Faculty of Medicine, University of Nagoya, Nagoya, Japan

Y. Tsukamoto Departments of Internal Medicine, and Biomedical Chemistry, Faculty of Medicine, University of Nagoya, Nagoya, Japan

S. Hase Departments of Internal Medicine, and Biomedical Chemistry, Faculty of Medicine, University of Nagoya, Nagoya, Japan

T. Arisawa Departments of Internal Medicine, and Biomedical Chemistry, Faculty of Medicine, University of Nagoya, Nagoya, Japan

T. Osada Departments of Internal Medicine, and Biomedical Chemistry, Faculty of Medicine, University of Nagoya, Nagoya, Japan

Y. Kawabe Departments of Internal Medicine, and Biomedical Chemistry, Faculty of Medicine, University of Nagoya, Nagoya, Japan

M. Kuroiwa Departments of Internal Medicine, and Biomedical Chemistry, Faculty of Medicine, University of Nagoya, Nagoya, Japan

T. Tsuchida Departments of Internal Medicine, and Biomedical Chemistry, Faculty of Medicine, University of Nagoya, Nagoya, Japan

T. Ozawa Departments of Internal Medicine, and Biomedical Chemistry, Faculty of Medicine, University of Nagoya, Nagoya, Japan

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Abstract

Four kinds of prostaglandins (PGs), 6-keto-PGF_1α, PGF_2α, PGE₂ and PGD₂, in rat gastric mucosa were decreased at 1 or 6 h after oral administration of indome-thacin (2 or 12 mg/kg). With 2 mg/kg of indomethacin, the PG levels had slightly recovered 6 h later. Gastric lesions were observed 6 h after administration of indomethacin (12 mg/kg), but not with 2 mg/kg. Omeprazole (20 mg/kg, i. p.) prevented ulcer formation caused by indomethacin, without improvement of the reduced gastric mucosal PG levels. PGD₂ (0.5 mg/kg, p. o.) reduced indomethacin-induced gastric lesions and considerable amounts of PGD₂ existed in the gastric mucosa. We conclude that H⁺ is a determining factor in the genesis of indomethacin-induced gastric lesions and persistent decreases in tissue PG levels also participate in ulcer formation.

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The Role of Prostaglandin D₂ in the Genesis of Indomethacin-Induced Gastric Lesions in Rats

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The Role of Prostaglandin D₂ in the Genesis of Indomethacin-Induced Gastric Lesions in Rats