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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 ＸⅡ）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 ＸⅡ 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 ＸⅡｍ 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 ＸⅡ 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 ＸⅡ 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 investigate the effects of dexamethasone (D E X) and aspirin on lipopolysaccharide (L P S) induced pulmonary capillary macrophage (P I M) cyclooxygenase Ⅱ (C O X Ⅱ) expression and activity. Methods: The improved method was isolated and cultured pig PMI. Divided into: ① control group; ② L P S group: L P S (10 μg / m l) stimulation; ③ D E X group and ④ A S A group: μmol / L A S A pretreatment 2 h, then L P S stimulation. Reverse transcription polymerase chain reaction and immunohistochemical staining were used to detect the changes of COX-Ⅱm R N A and enzyme protein. Radioimmunoassay was used to determine the concentration of P G E2 in the cell supernatant, which indirectly represented COX activity. Results: The expression of P I M COX X m R N A and P G E2 in L P S group was higher than that in control group, but decreased in D E X group (P <0.01) C O X Ⅱ m R N A and enzyme protein expression was similar to L P S group, but P G E2 concentration was decreased (P <0.01). CONCLUSION: D E X can inhibit L P S -induced P I M C O X II R N A and enzyme protein expression; A S A can reduce prostaglandin production by inhibiting C O X activity; both The treatment of acute inflammatory diseases such as acute respiratory distress syndrome may have a role.