TLR4/MD2复合物介导MyD88活化是卵巢上皮性癌（卵巢癌）紫杉醇耐药的重要分子机制之一。有证据显示，靶向阻断TLR4/MyD88通路能显著增强紫杉醇对MyD88+卵巢癌细胞微管蛋白的稳定性及细胞毒作用。我们前期研究发现，中药提取物6-姜烯酚可能是一种有效的TLR4/MD2复合物抑制剂，可阻断MyD88活化；另一方面，我们已制备出载6-姜烯酚相变纳米粒递药系统。MUC16(CA125)在MyD88+卵巢癌具有较高的膜表达表型，可增加纳米粒靶向性和卵巢癌组织分布。据此，本项目提出了“MUC16抗体耦合载6-姜烯酚相变纳米粒通过超声控释实现对MyD88+卵巢癌细胞靶向递药，从而阻断TLR4/MyD88通路介导的卵巢癌紫杉醇耐药”的假设，拟从分子、细胞水平和动物实验验证该靶向载药相变纳米粒能否改善卵巢癌紫杉醇治疗效应，为发展创新性的卵巢癌靶向治疗提供新思路和科学依据。

TLR4/MD2 complex-mediated activation of MyD88 is one of the major mechanism for paclitaxel chemoresistance in epithelial ovarian cancer (EOC). It is evidence that target-blocking TLR4/MyD88 pathway can significantly increase paclitaxel ability to stablize microtubules and enhance its cytotoxicity of in MyD88+ EOC cells. Our previous study found that the Chinese herbal extract 6-shogaol may be an effective TLR4/MD2 complex inhibitor that blocks the activation of MyD88. On the other hand, we have prepared a 6-shogaol phase transtion nanoparticles delivery system. MUC16 (CA125) has a high membrane expression in MyD88+ EOC, which can increase nanoparticles targeting and organizational distribution in EOC. Based on these findings, a hypothesis is proposed that Ultrasound triggered 6-shogaol release from MUC16 modified phase transtion nanoparticles for blocking TLR4/MyD88-dependent pathway mediated paclitaxel resistance in MyD88+ EOC. Through cell and animal experiment, we will verify whether the targeted drug-loaded phase transtion nanoparticles can sensitize the response of EOC to paclitaxel, in order to provide a scientific basis for development of a targeted therapy strategy of EOC.