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
[31]  
Subbaramaiah K, 1996, CANCER RES, V56, P4424
[32]   Hepatocyte growth factor as a key to modulate anti-ulcer action of prostaglandins in stomach [J].
Takahashi, M ;
Ota, S ;
Hata, Y ;
Mikami, Y ;
Azuma, N ;
Nakamura, T ;
Terano, A ;
Omata, M .
JOURNAL OF CLINICAL INVESTIGATION, 1996, 98 (11) :2604-2611
[33]  
TARNAWSKI A, 1991, MECHANISMS OF INJURY, PROTECTION AND REPAIR OF THE UPPER GASTROINTESTINAL TRACT, P521
[34]   QUALITY OF GASTRIC-ULCER HEALING - A NEW, EMERGING CONCEPT [J].
TARNAWSKI, A ;
STACHURA, J ;
KRAUSE, WJ ;
DOUGLASS, TG ;
GERGELY, H .
JOURNAL OF CLINICAL GASTROENTEROLOGY, 1991, 13 :S42-S47
[35]  
Tominaga K, 1998, DIGEST DIS SCI, V43, p134S
[36]   Increased expression of transforming growth factor-beta(1) during gastric ulcer healing in rats [J].
Tominaga, K ;
Arakawa, T ;
Kim, S ;
Iwao, H ;
Kobayashi, K .
DIGESTIVE DISEASES AND SCIENCES, 1997, 42 (03) :616-625
[37]   ALTERATIONS IN CELLULAR ADHESION AND APOPTOSIS IN EPITHELIAL-CELLS OVEREXPRESSING PROSTAGLANDIN-ENDOPEROXIDE-SYNTHASE-2 [J].
TSUJII, M ;
DUBOIS, RN .
CELL, 1995, 83 (03) :493-501
[38]  
TUJII M, 1997, P NATL ACAD SCI USA, V94, P3336
[39]   DELAYED HEALING OF ACETIC ACID-INDUCED GASTRIC-ULCERS IN RATS BY INDOMETHACIN [J].
WANG, JY ;
YAMASAKI, S ;
TAKEUCHI, K ;
OKABE, S .
GASTROENTEROLOGY, 1989, 96 (02) :393-402
[40]  
Watanabe T, 1997, AM J PATHOL, V150, P971