REGRESSION OF COLLAGEN-INDUCED ARTHRITIS WITH TAXOL, A MICROTUBULE STABILIZER
REGRESSION OF COLLAGEN-INDUCED ARTHRITIS WITH TAXOL, A MICROTUBULE STABILIZER
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DOI：
10.1002/art.1780370611
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发表时间：
1994-06-01
影响因子：
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通讯作者：
BANQUERIGO, ML
中科院分区：
文献类型：
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作者：
BRAHN, E;TANG, C;BANQUERIGO, ML
客观的。为了研究微管稳定剂紫杉醇的能力，抑制胶原蛋白诱导的关节炎（CIA），这是类风湿关节炎模型。用Li型胶原蛋白（第0天）对Louvain大鼠进行免疫，以诱导关节炎。紫杉醇是从第2天（预防方案）或第9天（在高剂量或低剂量抑制方案）开始的。在临床和射线照相上评估大鼠的关节炎严重程度。还评估了对II型胶原蛋白的细胞和体液免疫反应。关节炎发作之前的紫杉醇机构完全排除了中央情报局的发展（P <0.0001与对照组相比）。它还抑制了已建立的临床疾病（高剂量方案P <0.0000001；低剂量方案P <0.0001）和放射学侵蚀（高剂量方案P <0.00001;低剂量方案P <0.001）与对照组相比，IgG水平紫杉醇施用后，抗体，但不延迟型胶原蛋白的抗体。紫杉醇完全阻止了中央情报局的诱导，并导致现有关节炎的显着消退。
Objective. To investigate the capacity of taxol, a microtubule stabilizer, to inhibit collagen-induced arthritis (CIA), a model of rheumatoid arthritis.Methods. Louvain rats were immunized with type LI collagen (day 0) to induce arthritis. Taxol was administered beginning on day 2 (prevention protocol) or at arthritis onset on day 9 (in either a high-dose or low-dose suppression protocol). Rats were assessed clinically and radiographically for arthritis severity. Cellular and humoral immune responses to type II collagen were also evaluated.Results. Institution of taxol prior to arthritis onset completely precluded the development of CIA (P < 0.0001 versus controls). It also suppressed established clinical disease (high-dose protocol P < 0.0000001; low-dose protocol P < 0.0001) and radiographic erosions (high-dose protocol P < 0.00001; low-dose protocol P < 0.001) compared with controls, Levels of IgG antibodies, but not delayed-type hypersensitivity, to type II collagen were reduced after taxol administration.Conclusion. Taxol completely prevented the induction of CIA and caused significant regression of existing arthritis.