Wolberg G, Stopford C R, Zimmerman T P
Proc Natl Acad Sci U S A. 1984 Jun;81(11):3496-500. doi: 10.1073/pnas.81.11.3496.
Several microtubule-disrupting agents (colchicine, demecolcine, vinblastine, vincristine, podophyllotoxin, and nocodazole) have been shown to inhibit lymphocyte-mediated cytolysis. These agents also enhanced the prostaglandin E1-induced rise in cAMP levels in these cytolytic lymphocytes. Taxol, a natural product alkaloid that has been shown to enhance microtubule polymerization and to stabilize microtubules, antagonized both of these effects of the microtubule-disrupting agents in the cytolytic lymphocytes. Taxol also antagonized the enhancement of cAMP increases by colchicine in lymphocytes stimulated by 2-chloroadenosine, isoproterenol, and cholera toxin. The enhancement of the prostaglandin E1-induced cAMP response caused by treatment of the lymphocytes with either cytochalasin B or 3-deazaadenosine in the presence or absence of L-homocysteine was not antagonized by taxol. Taxol, colchicine, or the combination of these two agents did not affect ATP levels in cytolytic lymphocytes. These results support a modulatory role for microtubules in both the cytolytic process and the production of cAMP in these lymphocytes.
几种破坏微管的药物(秋水仙碱、去甲秋水仙碱、长春花碱、长春新碱、鬼臼毒素和诺考达唑)已被证明可抑制淋巴细胞介导的细胞溶解。这些药物还增强了前列腺素E1诱导的这些溶细胞性淋巴细胞中cAMP水平的升高。紫杉醇是一种天然产物生物碱,已被证明可增强微管聚合并稳定微管,它拮抗了破坏微管药物在溶细胞性淋巴细胞中的这两种作用。紫杉醇还拮抗了秋水仙碱对2-氯腺苷、异丙肾上腺素和霍乱毒素刺激的淋巴细胞中cAMP增加的增强作用。在有或没有L-同型半胱氨酸存在的情况下,用细胞松弛素B或3-脱氮腺苷处理淋巴细胞所引起的前列腺素E1诱导的cAMP反应增强不受紫杉醇的拮抗。紫杉醇、秋水仙碱或这两种药物的组合不影响溶细胞性淋巴细胞中的ATP水平。这些结果支持微管在这些淋巴细胞的细胞溶解过程和cAMP产生中起调节作用。