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地塞米松和阿斯匹林对猪肺血管内巨噬细胞环氧合酶Ⅱ型的作用 被引量:1

Effects of dexamethasone and aspirin on cyclooxygenase Ⅱ in porcine pulmonary intravascular macrophages stimulated with lipopolysaccharide
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摘要 目的:探讨地塞米松( D E X)和阿斯匹林( A S A)对脂多糖( L P S)致猪肺血管内巨噬细胞( P I M)环氧合酶Ⅱ( C O XⅡ)表达及活性的影响。方法:改良法分离、培养猪 P I M。分为:①对照组;② L P S组:予 L P S(10 μg/m l)刺激;③ D E X 组和④ A S A 组:分别以2 μm ol/ L D E X和500 μm ol/ L A S A 预处理2 h,再以 L P S刺激。以反转录聚合酶链反应和免疫组化染色法检测 C O XⅡ m R N A 及酶蛋白的改变;放射免疫分析法测定细胞上清 P G E2 浓度,间接表示 C O X活性。结果: L P S组 P I M C O XⅡm R N A 和酶蛋白表达及 P G E2浓度较对照组升高, D E X组则降低( P< 0.01); A S A 组 C O XⅡ m R N A 和酶蛋白表达与 L P S组相似,但 P G E2 浓度却降低( P < 0.01)。结论: D E X能抑制 L P S诱导的 P I M C O XⅡ m R N A 及酶蛋白的表达; A S A可通过抑制 C O X的活性而减少前列腺素的产生;二者对急性呼吸窘迫综合征等急性炎症性疾病的治疗可能有一定作用。 Objective: To study the effects of dexamethasone (DEX) and acetylsalicylic acid (ASA) on the expression and activity of cyclooxygenase Ⅱ (COX Ⅱ) in porcine pulmonary intravascular macrophages (PIM) stimulated with lipopolysaccharide (LPS). Methods: Isolated porcine PIM were cultured and divided into the control group; LPS stimulated group of which the PIM were stimulated with LPS (10 μg/ml); DEM or ASA treated groups of which the PIM were pre cultured with DEX (2 μmol/L) or ASA (500 μmol/L) 2 h prior to LPS stimulation. The changes of COX Ⅱ mRNA were determined with reverse transcription polymerase chain reaction (RT PCR) and those of COX Ⅱ protein with immunohistochemistry. The level of prostaglandin E 2 (PGE 2), which serves to express the activity of COX Ⅱ, in the supernatant of PIM was measured with radio immunoassay (RIA). Results: COX Ⅱ mRNA expression, COX Ⅱ protein and PGE 2 level were significantly higher in LPS group than in the control but lower in DEX treated group than in LPS group ( P <0.01). In ASA group, the changes of COX Ⅱ mRNA expression and COX Ⅱ protein were similar to those of LPS group but PGE 2 level was significantly lower (P<0.01). Conclusion: DEX can inhibit the expression of COX Ⅱ mRNA and COX Ⅱ protein after LPS stimulation of porcine PIM and ASA can only inhibit the activity of COX Ⅱ by showing the decrease of PGE 2. Both DEX and ASA may exert certain therapeutic effects on acute inflammatory diseases such as acute respiratory distress syndrome.
出处 《第三军医大学学报》 CAS CSCD 北大核心 1999年第9期634-637,共4页 Journal of Third Military Medical University
基金 国家自然科学基金
关键词 呼吸窘迫 PIM 地塞米松 阿斯匹林 COX-II pulmonary intravascular macrophage cyclooxygenase Ⅱ lipopolysaccharide dexamethasone aspirin
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  • 1李胜亮,国外医学.呼吸系统分册,1996年,16卷,197页 被引量:1
  • 2徐剑铖,中国病理生理杂志,1996年,12卷,495页 被引量:1

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