论文部分内容阅读
氨甲酰胆碱(CCh)可使事先以[~3H]花生四烯酸充分标记的CCL137细胞释放的花生四烯酸量明显增多,经CCh处理的CCL137细胞,其质膜中磷脂酶A_2(PLA_2)的活性明显增高;PLA_2及其激活剂蜂毒肽都能像CCh处理一样,降低CCL137细胞与[~3H]NMS的结合作用;PLA_2的非竞争性抑制剂米帕林能有效地减轻CCh所致细胞对[~3H]NMS结合的降低,以上结果表明,质膜中PLA_2激活可能在CCh所致CCL137细胞的M-受体隐没中起重要作用,PLA2激活还与CCh所致CCL137细胞中磷脂酰肌醇代谢增强有关。
Carbachyl (CCh) significantly increased the amount of arachidonic acid released by CCL137 cells pre-labeled with [~ 3H] arachidonic acid. CCL-treated CCL137 cells showed a significant increase in phospholipase A_2 The activity of PLA_2 was significantly increased. Both PLA_2 and its activator melittin could reduce the binding of CCL137 cells to [~ 3H] NMS, as did CCh treatment. The non-competitive inhibitor of melphalan, PLA 2, effectively reduced the activity of CCh The results indicated that PLA 2 activation in plasma membrane may play an important role in M-receptor occlusion of CCL 137 cells induced by CCh, and PLA 2 activation is also associated with CCh-induced CCL 137 cells Phosphatidylinositol metabolism related to increased.