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佐剂诱导性关节炎大鼠腹膜巨噬细胞的类二十烷酸生成及磷脂酶A2分泌

Eicosanoid production and phospholipase A2 secretion by peritoneal macrophages from rats with adjuvant-induced arthritis.

作者信息

Bak C E, Anderson C M, Hanglow A C, Morgan D W

机构信息

Department of Pharmacology, Hoffmann-La Roche Inc., Nutley, NJ 07110-1199.

出版信息

Agents Actions. 1991 Sep;34(1-2):81-3. doi: 10.1007/BF01993244.

Abstract

The effect of adjuvant-induced arthritis on rat peritoneal macrophage (RPM) function with respect to [14C]arachidonic acid (AA) release, leukotriene B4 (LTB4) and prostaglandin E2 (PGE2) production, and secreted phospholipase A2 (PLA2) activity was investigated. Twice as many cells were lavaged from the peritoneal cavity of arthritic rats 21 days post-adjuvant injection than were lavaged from normal rats. PGE2 production was increased two-fold in Ca++ ionophore-stimulated RPM from the adjuvant animals as compared with RPM from control animals. However, PLA2 secretion, LTB4 production and [14C]AA release were unchanged. These results suggest that PGE2 production, rather than LTB4 production or PLA2 secretion, is preferentially enhanced in Ca++ ionophore-stimulated RPM from arthritic rats and may, therefore, reflect a major role for PGE2 in adjuvant-induced arthritis. However, the presence of increase numbers of macrophages and their associated products, including PLA2 and LTB4, may also contribute to the inflammatory process in this disease.

摘要

研究了佐剂诱导的关节炎对大鼠腹腔巨噬细胞(RPM)功能的影响,涉及[14C]花生四烯酸(AA)释放、白三烯B4(LTB4)和前列腺素E2(PGE2)生成以及分泌型磷脂酶A2(PLA2)活性。在佐剂注射后21天,从患有关节炎大鼠的腹腔冲洗出的细胞数量是正常大鼠的两倍。与对照动物的RPM相比,佐剂动物经钙离子载体刺激的RPM中PGE2生成增加了两倍。然而,PLA2分泌、LTB4生成和[14C]AA释放未发生变化。这些结果表明,在经钙离子载体刺激的关节炎大鼠RPM中,PGE2生成而非LTB4生成或PLA2分泌优先增强,因此可能反映了PGE2在佐剂诱导的关节炎中的主要作用。然而,巨噬细胞及其相关产物(包括PLA2和LTB4)数量的增加也可能对该疾病的炎症过程有贡献。

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