解热镇痛药同样抑制星形胶质细胞和巨噬细胞释放前列腺素。

Antipyretic analgesics inhibit prostaglandin release from astrocytes and macrophages similarly.

作者信息

Lanz R, Polster P, Brune K

出版信息

Eur J Pharmacol. 1986 Oct 14;130(1-2):105-9. doi: 10.1016/0014-2999(86)90188-3.

Abstract

The effect of acid and non-acid antipyretic analgesics on prostaglandin (PG) release from cultured mouse astrocytes and peritoneal macrophages was investigated in order to test the hypothesis that the non-acid compounds are more potent inhibitors of PG formation in brain than in peripheral tissues. Stimulation of the cells by the divalent cation ionophore A 23187 (10(-6) mol/l) induced PG release from astrocytes and macrophages (mainly PGD2 and PGE2, respectively). This PG release was inhibited by acetylsalicylic acid (10(-5) - 10(-6) mol/l) and indomethacin (10(-6) - 10(-9) mol/l) but also by high concentrations (10(-3) - 10(-5) mol/l) of the non-acid compounds 4-methyl-aminophenazone, the main active metabolite of dipyrone (metamizol), and acetaminophen (paracetamol). No difference was found in the inhibitory potency of the drugs in astrocytes and macrophages, suggesting that a specific sensitivity of brain cells toward non-acid antipyretic analgesics does not contribute to their analgesic effect.

摘要

为了验证非酸性化合物在脑中比在周围组织中对前列腺素（PG）形成的抑制作用更强这一假说，研究了酸性和非酸性解热镇痛药对培养的小鼠星形胶质细胞和腹腔巨噬细胞释放PG的影响。二价阳离子载体A 23187（10⁻⁶mol/L）刺激细胞可诱导星形胶质细胞和巨噬细胞释放PG（分别主要为PGD₂和PGE₂）。这种PG释放受到阿司匹林（10⁻⁵ - 10⁻⁶mol/L）和吲哚美辛（10⁻⁶ - 10⁻⁹mol/L）的抑制，但也受到高浓度（10⁻³ - 10⁻⁵mol/L）的非酸性化合物4-甲基氨基苯酮、双氯芬酸（甲灭酸）的主要活性代谢物以及对乙酰氨基酚（扑热息痛）的抑制。未发现药物对星形胶质细胞和巨噬细胞的抑制效力存在差异，这表明脑细胞对非酸性解热镇痛药的特异性敏感性与其镇痛作用无关。