Rescue strategies against non-steroidal anti-inflammatory drug-induced gastroduodenal damage

被引:31
作者
Lim, Yun Jeong [2 ]
Lee, Jeong Sang
Ku, Yang Suh
Hahm, Ki-Baik [1 ]
机构
[1] Gachon Univ Med & Sci, Dept Gastroenterol, Lab Translat Med, Lee Gil Ya Canc & Diabet Inst, Inchon 406840, South Korea
[2] Dongguk Univ, Dept Internal Med, Ilsan Hosp, Coll Med, Goyang, South Korea
关键词
cyclooxygenase; gastroduodenal damage; non-steroidal anti-inflammatory drug; safety; UNFOLDED PROTEIN RESPONSE; MITOCHONDRIAL OXIDATIVE-PHOSPHORYLATION; GASTRIC EPITHELIAL-CELLS; ZINC ACEXAMATE; INDUCED APOPTOSIS; HYDROGEN-SULFIDE; ER STRESS; GASTROINTESTINAL COMPLICATIONS; GASTROPROTECTIVE STRATEGIES; LIPID MEDIATORS;
D O I
10.1111/j.1440-1746.2009.05929.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Non-steroidal anti-inflammatory drugs (NSAIDs) are the most commonly prescribed drugs worldwide, which attests to their efficacy as analgesic, antipyretic and anti-inflammatory agents as well as anticancer drugs. However, NSAID use also carries a risk of major gastroduodenal events, including symptomatic ulcers and their serious complications that can lead to fatal outcomes. The development of "coxibs" (selective cyclooxygenase-2 [COX-2] inhibitors) offered similar efficacy with reduced toxicity, but this promise of gastroduodenal safety has only partially been fulfilled, and is now dented with associated risks of cardiovascular or intestinal complications. Recent advances in basic science and biotechnology have given insights into molecular mechanisms of NSAID-induced gastroduodenal damage beyond COX-2 inhibition. The emergence of newer kinds of NSAIDs should alleviate gastroduodenal toxicity without compromising innate drug efficacy. In this review, novel strategies for avoiding NSAID-associated gastroduodenal damage will be described.
引用
收藏
页码:1169 / 1178
页数:10
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