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七十年代把NSAIDs的抗炎效应归因于抑制内源性前列腺素的产生,随着对前列腺素E(PGE)免疫调节作用的日趋了解,提出了NSAIDs是否通过抑制PGE的产生,而直接影响免疫功能的问题.除成熟红细胞外的所有组织均可产生前列腺素E_2(PGE_2),人类外周血生成PGE_2的细胞是单核细胞,PGE_2对免疫功能具有抑制作用,如抑制体外T细胞促有丝分裂原反应、克隆增殖、抗原刺激、E花环形成、产生淋巴因子(包括白细胞间介素2)等.
Seventies attributed anti-inflammatory effects of NSAIDs to the inhibition of endogenous prostaglandin production. With the increasing understanding of the immunomodulatory effects of prostaglandin E (PGE), it was proposed whether NSAIDs directly affect the production of PGE by suppressing the production of PGE Immune function of all tissues except mature red blood cells can produce prostaglandin E_2 (PGE_2), human peripheral blood PGE_2 cells are monocytes, PGE_2 on immune function, such as inhibition of T cell mitogen Reaction, clonal proliferation, antigen stimulation, E rosette formation, production of lymphokines (including interleukin 2) and the like.