中国综合临床
中國綜閤臨床
중국종합림상
CLINICAL MEDICINE OF CHINA
2013年
4期
358-360
,共3页
张志广%陆伟%李熳%闻淑军%季英兰%夏秀丽
張誌廣%陸偉%李熳%聞淑軍%季英蘭%夏秀麗
장지엄%륙위%리만%문숙군%계영란%하수려
非甾体抗炎药%血管内皮生长因子%丙二醛%缺氧诱导因子-1α
非甾體抗炎藥%血管內皮生長因子%丙二醛%缺氧誘導因子-1α
비치체항염약%혈관내피생장인자%병이철%결양유도인자-1α
Non-steroidal anti-inflammatory drug%Vascular endothelial growth factor%Malondialdehyde%Hypoxia inducible factor-1α
目的 探讨非甾体抗炎药(NSAID)相关胃黏膜损伤组织中血管内皮生长因子(VEGF)、丙二醛、缺氧诱导因子-1α(HIF-1α)的表达,进而了解NSAID引起胃黏膜损伤的作用机制.方法 收集我院内镜室胃黏膜活检标本114份,其中来自服用NSAID的慢性胃炎伴糜烂及胃溃疡患者70例(NSAID组),余44份标本来自未服用NSAID的慢性浅表性胃炎患者(对照组),应用免疫组织化学方法检测两组胃黏膜组织中VEGF、丙二醛、HIF-1α,结果以阳性率表示.结果 NSMD组VEGF阳性表达率明显低于对照组[25.7％ (18/70)与54.5％ (24/44),x2=9.70]；而丙二醛和HIF-1α的阳性率明显高于对照组[62.9％ (44/70)与27.3％ (12/44),x2=13.70;45.7％ (32/70)与13.6％ (6/44),x2=12.50],差异均有统计学意义(P均＜0.05).结论 NSAID药物可能通过降低胃黏膜组织中的VEGF及升高丙二醛、HIF1-α而引起胃黏膜组织的损伤.
目的 探討非甾體抗炎藥(NSAID)相關胃黏膜損傷組織中血管內皮生長因子(VEGF)、丙二醛、缺氧誘導因子-1α(HIF-1α)的錶達,進而瞭解NSAID引起胃黏膜損傷的作用機製.方法 收集我院內鏡室胃黏膜活檢標本114份,其中來自服用NSAID的慢性胃炎伴糜爛及胃潰瘍患者70例(NSAID組),餘44份標本來自未服用NSAID的慢性淺錶性胃炎患者(對照組),應用免疫組織化學方法檢測兩組胃黏膜組織中VEGF、丙二醛、HIF-1α,結果以暘性率錶示.結果 NSMD組VEGF暘性錶達率明顯低于對照組[25.7％ (18/70)與54.5％ (24/44),x2=9.70]；而丙二醛和HIF-1α的暘性率明顯高于對照組[62.9％ (44/70)與27.3％ (12/44),x2=13.70;45.7％ (32/70)與13.6％ (6/44),x2=12.50],差異均有統計學意義(P均＜0.05).結論 NSAID藥物可能通過降低胃黏膜組織中的VEGF及升高丙二醛、HIF1-α而引起胃黏膜組織的損傷.
목적 탐토비치체항염약(NSAID)상관위점막손상조직중혈관내피생장인자(VEGF)、병이철、결양유도인자-1α(HIF-1α)적표체,진이료해NSAID인기위점막손상적작용궤제.방법 수집아원내경실위점막활검표본114빈,기중래자복용NSAID적만성위염반미란급위궤양환자70례(NSAID조),여44빈표본래자미복용NSAID적만성천표성위염환자(대조조),응용면역조직화학방법검측량조위점막조직중VEGF、병이철、HIF-1α,결과이양성솔표시.결과 NSMD조VEGF양성표체솔명현저우대조조[25.7％ (18/70)여54.5％ (24/44),x2=9.70]；이병이철화HIF-1α적양성솔명현고우대조조[62.9％ (44/70)여27.3％ (12/44),x2=13.70;45.7％ (32/70)여13.6％ (6/44),x2=12.50],차이균유통계학의의(P균＜0.05).결론 NSAID약물가능통과강저위점막조직중적VEGF급승고병이철、HIF1-α이인기위점막조직적손상.
Objective To study the expression of Vascular Endothelial Growth Factor (VEGF),Malondialdehyde (MDA),Hypoxia Inducible Factor-1 α (HIF-1 α) in the Non-Steroidal Anti-Inflammatory Drug (NSAID)-associated gastric mucosa injury tissue,and to understand the mechanism of NSAID induced gastric mucosa injury.Methods We collected 114 biopsy specimen of gastric mucosa under endoscope from patients admitted to our hospital,including 70 cases with NSAID-associated chronic erosive gastritis or gastric ulcer (NSAID group) and 44 cases with chronic superficial gastritis who never take NSAID as controls (the control group).Immunohistochemistry technique was used to detect the positive expressions of VEGF,MDA,HIF-1α in patients.Results The positive rate of VEGF expression in the NSADI group was significantly lower than that in the normal control group (25.7％ (18/70) vs.54.5％ (24/44),x2 =9.70,P ＜ 0.05).The positive rates of MDA and HIF-1α in the NSADI group were significantly higher than these in the normal control group (MDA:62.9％ (44/70) vs.27.3％ (12/44),x2 =13.70,P ＜0.05; HIF-1α:45.7％ (32/70) vs.13.6％ (6/44),x2 =12.50,P ＜ 0.05).Conclusion NSAID drugs may induce gastric mucosa injury by decreasing the expression of VEGF and increase the levels of MDA and HIF1-α in gastric mucosa tissue.
