West Sonlee D, Suliburk James W, Smith Gregory S, Mercer David W
Department of Surgery, University of Texas Medical School, Houston, Texas, 77030, USA.
Dig Dis Sci. 2006 Apr;51(4):754-65. doi: 10.1007/s10620-006-3203-2.
This study was done to examine the role of cyclooxygenase (COX) in lipopolysaccharide (LPS)-induced gastroprotection and gastric stasis. In conscious rats, LPS dose and time dependently increased gastric luminal fluid accumulation. LPS decreased blood flow (laser Doppler) and prevented gastric injury from acidified ethanol at time points before significant fluid accumulation occurred. LPS increased COX-2 but not COX-1 expression. In contrast, LPS decreased gastric mucosal prostaglandin synthesis. LPS-induced gastric luminal fluid accumulation was negated by both nonselective COX inhibition with salicylate and selective COX-2 inhibition with NS-398 but not by selective COX-1 inhibition with SC-560. Neither salicylate nor NS-398 blocked LPS-induced gastroprotection. LPS-induced gastroprotection does not depend entirely on accumulation of luminal fluid and is independent of COX-1 and COX-2. However, the ability of LPS to cause gastric stasis and increase gastric luminal fluid accumulation involves COX-2.
本研究旨在探讨环氧化酶（COX）在脂多糖（LPS）诱导的胃保护和胃淤滞中的作用。在清醒大鼠中，LPS剂量和时间依赖性地增加胃腔液积聚。在显著的液体积聚发生之前的时间点，LPS降低血流量（激光多普勒）并预防酸化乙醇引起的胃损伤。LPS增加COX-2的表达，但不增加COX-1的表达。相反，LPS降低胃黏膜前列腺素的合成。LPS诱导的胃腔液积聚被水杨酸非选择性抑制COX和NS-398选择性抑制COX-2所消除，但不被SC-560选择性抑制COX-1所消除。水杨酸和NS-398均未阻断LPS诱导的胃保护作用。LPS诱导的胃保护作用并不完全依赖于腔液的积聚，且独立于COX-1和COX-2。然而，LPS导致胃淤滞和增加胃腔液积聚的能力涉及COX-2。
