人类自发单核细胞介导的细胞毒性药理学。I. 水杨酸盐和类固醇的增强作用。
Pharmacology of human spontaneous monocyte-mediated cytotoxicity. I. Enhancement by salicylates and steroids.
作者信息
Kleinerman E S, Louie J S, Wahl L M, Muchmore A V
出版信息
Arthritis Rheum. 1981 Jun;24(6):774-80. doi: 10.1002/art.1780240604.
The effect of various antiinflammatory agents on the spontaneous cytotoxicity of human mononuclear cells in vitro was assessed. Acetylsalicylic acid (ASA) and hydrocortisone enhanced spontaneous monocyte-mediated cytotoxicity compared to control values. This enhancement could not be mediated through inhibition of prostaglandin biosynthesis since indomethacin had no effect on cytotoxic function and since the direct addition of PGE2 to the cell cultures did not inhibit the expression of cytotoxicity. Likewise, salicylic acid (SA), which had no effect on prostaglandin biosynthesis, also enhanced monocyte cytotoxicity. Stimulation of monocyte-mediated cytotoxicity resulting in more efficient antigen removal and thus decreasing antigen persistence may be an additional mechanism by which ASA, SA, and hydrocortisone modulate the destructive inflammatory response in rheumatoid arthritis.
评估了多种抗炎剂对人单核细胞体外自发细胞毒性的影响。与对照值相比，乙酰水杨酸（ASA）和氢化可的松增强了自发单核细胞介导的细胞毒性。这种增强不能通过抑制前列腺素生物合成来介导，因为吲哚美辛对细胞毒性功能没有影响，并且因为直接向细胞培养物中添加PGE2不会抑制细胞毒性的表达。同样，对前列腺素生物合成没有影响的水杨酸（SA）也增强了单核细胞毒性。刺激单核细胞介导的细胞毒性导致更有效地清除抗原，从而减少抗原持久性，这可能是ASA、SA和氢化可的松调节类风湿性关节炎中破坏性炎症反应的另一种机制。
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