Prostaglandins in the stomach: An update

被引:30
作者
Arakawa, T
Higuchi, K
Fukuda, T
Fujiwara, Y
Kobayashi, K
Kuroki, T
机构
[1] Osaka City Univ, Sch Med, Dept Internal Med 3, Abeno Ku, Osaka 545, Japan
[2] Osaka City Univ, Sch Med, Dept Biosignal Anal, Abeno Ku, Osaka 545, Japan
关键词
prostaglandins; gastric mucosa; cytokine; nonsteroidal antiinflammatory drugs; Helicobacter pylori; quality of ulcer healing; ulcer recurrence; cyclooxygenase; gastric carcinoma;
D O I
10.1097/00004836-199800001-00003
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Prostaglandins (PGs) are responsible for regulation of various physiologic activities in many tissues and organs, including the stomach. Recent studies have shown new crucial roles of PGs in the stomach. Activation of inflammatory cytokines and neutrophils may cause acute gastric mucosal lesions and recurrence of ulcers, which are induced by noxious stimuli such as nonsteroidal antiinflammatory drugs (NSAIDs), stress and Helicobacter pylori (H. pylori). These phenomena are PC-dependent because exogenous PGs reverse them. PG deficiency and H. pylori may worsen the quality of ulcer healing in terms of inflammatory responses, which are related to future ulcer recurrence. Neutrophils, monocytes/macrophages, and adhesion molecules are involved in the mechanism of recurrence caused by inflammatory cytokines. PGs accelerate ulcer healing, possibly via angiogenesis, epithelial cell proliferation, production of growth factors such as hepatocyte growth factor and transforming growth factor beta, reconstruction of extracellular matrices, and suppression of inflammatory cell infiltration, in addition to gastroprotective mechanisms. The PG synthase cyclooxygenase (COX) has two forms, COX-1 and COX-2. COX-2, but not COX-1, contributes to ulcer healing. Moreover, recent studies suggest the involvement of COX-2 in development of gastric and colon carcinoma. This may be linked to the chemopreventive effect of NSAIDs.
引用
收藏
页码:S1 / S11
页数:11
相关论文
共 40 条
[1]   Tumor necrosis factor mediation of NSAID-induced gastric damage: Role of leukocyte adherence [J].
Appleyard, CB ;
McCafferty, DM ;
Tigley, AW ;
Swain, MG ;
Wallace, JL .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 1996, 270 (01) :G42-G48
[2]   Indomethacin treatment during initial period of acetic acid-induced rat gastric ulcer healing promotes persistent polymorphonuclear cell-infiltration and increases future ulcer recurrence - Possible mediation of prostaglandins [J].
Arakawa, T ;
Watanabe, T ;
Fukuda, T ;
Higuchi, K ;
Takaishi, O ;
Yamasaki, K ;
Kobayashi, K ;
Tarnawski, A .
DIGESTIVE DISEASES AND SCIENCES, 1996, 41 (10) :2055-2061
[3]  
ARAKAWA T, 1993, EUR J GASTROEN HEPAT, V5, pS87
[4]  
ARAKAWA T, 1981, Gastroenterologia Japonica, V16, P236
[5]   DEFICIENCY OF ENDOGENOUS PROSTANOIDS IN GASTRIC AND DUODENAL-ULCER DISEASES [J].
ARAKAWA, T ;
NAKAMURA, H ;
SATOH, H ;
FUKUDA, T ;
SAKUMA, H ;
KOBOYASHI, K .
JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, 1988, 3 (05) :441-449
[6]   GASTRIC INJURY AND INVASION OF PARIETAL-CELLS BY SPIRAL BACTERIA IN RHESUS-MONKEYS - ARE GASTRITIS AND HYPERCHLORHYDRIA INFECTIOUS-DISEASES [J].
DUBOIS, A ;
TARNAWSKI, A ;
NEWELL, DG ;
FIALA, N ;
DABROS, W ;
STACHURA, J ;
KRIVAN, H ;
HEMANACKAH, LM .
GASTROENTEROLOGY, 1991, 100 (04) :884-891
[7]   Increased cyclooxygenase-2 levels in carcinogen-induced rat colonic tumors [J].
DuBois, RN ;
Radhika, A ;
Reddy, BS ;
Entingh, AJ .
GASTROENTEROLOGY, 1996, 110 (04) :1259-1262
[8]   UP-REGULATION OF CYCLOOXYGENASE-2 GENE-EXPRESSION IN HUMAN COLORECTAL ADENOMAS AND ADENOCARCINOMAS [J].
EBERHART, CE ;
COFFEY, RJ ;
RADHIKA, A ;
GIARDIELLO, FM ;
FERRENBACH, S ;
DUBOIS, RN .
GASTROENTEROLOGY, 1994, 107 (04) :1183-1188
[9]  
Fujiwara Y, 1993, J Physiol Pharmacol, V44, P147
[10]   ROLES OF ENDOGENOUS LEUKOTRIENES AND PROSTAGLANDINS IN THE HEALING OF GASTRIC-ULCERS INDUCED BY ACETIC-ACID IN RATS [J].
FUKUDA, T ;
ARAKAWA, T ;
TORII, Y ;
NEBIKI, H ;
NAKAMURA, H ;
KOBAYASHI, K .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 1989, 24 :2-5