Department of Obstetrics and Gynecology, Shanghai Jiaotong University-Affiliated Sixth People's Hospital of Fengxian Branch, Shanghai, China.
Eur Rev Med Pharmacol Sci. 2013 Nov;17(21):2902-8.
Recent studies showed that dexamethasone (DEX) could render cancer cells resistant to paclitaxel (PTX) induced apoptosis though an unknown mechanism.
This study aimed to evaluate the influence of DEX pretreatment on the anti-tumor effect of PTX in an in vivo xenograft model with grafted ovarian cancer SKOV-3 cells innude mice.
The xenograft procedure was performed, and the nude mice were grouped into four cohorts of ten that received the following treatments: Control group, DEX group, PTX group and DEX+PTX group. Individual treatments were administered once every three days for a total of 6 courses. The growth of tumors and the inhibition rates were measured. Changes in tissue morphology and cellular ultrastructure were observed using light and transmission electron microscopy. Immunohistochemistry was performed to examine the expression of Ki-67, Bcl-xL and cleaved caspase-3.
Premedication with DEX reduced the inhibitory effect of PTX on tumor growth by approximately 20% compared to the PTX-only-treated group in the ovarian carcinoma xeno-grafted mice. Hematoxylin-eosin (H&E) staining revealed that significantly fewer cells exhibited vacuolization and apoptosis in the DEX + PTX group compared to the PTX group. Apoptotic characteristics including karyopyknosis, nuclear chromatin condensation along the nuclear membrane and aggregation were observed in both DEX+PTX and PTX groups under electron microscopy. However, these characteristics were less significant in the DEX+PTX group than those in the PTX group. The immunohistochemistry demonstrated that protein expression levels of Ki-67 and Bcl-xL were significantly increased, whereas cleaved caspase-3 decreased in the DEX+PTX group, compared to PTX group (p < 0.0125).
DEX inhibits the therapeutic efficacy of PTX in a human ovarian carcinoma SKOV-3 xenograft model.
最近的研究表明，地塞米松（DEX）通过未知机制使癌细胞对紫杉醇（PTX）诱导的细胞凋亡产生抗性。
本研究旨在评估 DEX 预处理对荷卵巢癌 SKOV-3 细胞裸鼠体内模型中 PTX 抗肿瘤作用的影响。
进行异种移植程序，将裸鼠分为四组，每组 10 只，分别接受以下治疗：对照组、DEX 组、PTX 组和 DEX+PTX 组。个体治疗每三天进行一次，共进行 6 个疗程。测量肿瘤的生长和抑制率。使用光镜和透射电镜观察组织形态和细胞超微结构的变化。免疫组织化学检测 Ki-67、Bcl-xL 和 cleaved caspase-3 的表达。
与仅用 PTX 治疗的组相比，预先用 DEX 治疗使荷卵巢癌裸鼠模型中 PTX 对肿瘤生长的抑制作用降低了约 20%。苏木精-伊红（H&E）染色显示，DEX+PTX 组与 PTX 组相比，细胞空泡化和凋亡明显减少。电镜下观察到 DEX+PTX 和 PTX 组均出现核固缩、核染色质沿核膜浓缩和聚集等凋亡特征。然而，DEX+PTX 组的这些特征明显比 PTX 组少。免疫组织化学显示，DEX+PTX 组 Ki-67 和 Bcl-xL 的蛋白表达水平明显升高，而 cleaved caspase-3 降低，与 PTX 组相比（p < 0.0125）。
DEX 抑制了人卵巢癌 SKOV-3 异种移植模型中 PTX 的治疗效果。
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