Li J, Jiang Y Y, Yue T L
Zhongguo Yao Li Xue Bao. 1989 May;10(3):274-8.
[3H]Arachidonic acid (AA)-prelabeled mouse peritoneal macrophages were stimulated by calcium ionophore A-23187 to release [3H]AA metabolites. The major labeled products which were co-chromatographed with the authentic PG and LT standards by TLC and determined by liquid scintillation were 6-keto-PGF1 alpha, PGE2, LTC4, and LTB4. Anisodamine (Ani) significantly inhibited the A-23187-induced release of PG and LT from mouse macrophages in a dose-dependent manner. In the presence of Ani at 0.5 mmol/L, the A-23187-induced release of 6-keto-PGF1 alpha, PGE2, LTC4 and LTB4 was reduced by 57%, 20%, 53% and 49%, respectively. A-23187-induced release of 6-keto-PGF1 alpha measured by RIA from bovine aorta endothelial cells was also significantly inhibited by Ani in a dose-dependent manner. These results indicate that the calcium-antagonistic effects of Ani may not only play a significant role in its inhibiting release of PG and LT, but also contribute to its salutary effects in the treatment of septic shock.
用[3H]花生四烯酸（AA）预标记的小鼠腹腔巨噬细胞，经钙离子载体A - 23187刺激后释放[3H]AA代谢产物。通过薄层层析（TLC）与真实的前列腺素（PG）和白三烯（LT）标准品共层析，并通过液体闪烁测定法确定的主要标记产物为6 - 酮 - PGF1α、PGE2、LTC4和LTB4。山莨菪碱（Ani）以剂量依赖的方式显著抑制A - 23187诱导的小鼠巨噬细胞中PG和LT的释放。在0.5 mmol/L的Ani存在下，A - 23187诱导的6 - 酮 - PGF1α、PGE2、LTC4和LTB4的释放分别减少了57%、20%、53%和49%。放射免疫分析法（RIA）测定显示，Ani也以剂量依赖的方式显著抑制A - 23187诱导的牛主动脉内皮细胞中6 - 酮 - PGF1α的释放。这些结果表明，Ani的钙拮抗作用可能不仅在其抑制PG和LT释放中起重要作用，而且有助于其在感染性休克治疗中的有益作用。
