载地塞米松磷酸钠洗脱微球靶向肝癌介入栓塞后炎症反应的机制研究

Transcatheter arterial chemoembolization is the main method for the treatment of advanced hepatocellular carcinoma. However, embolization can not achieve total necrosis of tumor tissues, and the residual tumor cells has become an important source of metastasis and recurrence following embolization. The inflammation in the residual tumor and adjacent tissues t promotes the tumor microenvironment change. It is well-known that the inflammation makes tumor cell survival, invasion and metastasis. Therefore, we speculated that the inflammation after embolic therapy may be one of the key factors for residual tumor tissues. We found that the inflammation after the embolization may be associated with the angiogenesis of the residual tumor tissues in the preliminary experimental study. The relevant mechanism needs to be explored further. Thus, we plan to research whether the inflammation in the residual tumor tissues and adjacent tissues is involved the angiogenesis, cell proliferation and metabolism of the residual tumors with VX2 rabbit liver cancer model. The eluting microspheres DC-Bead loading dexamethasone sodium phosphate can release dexamethasone sodium phosphate with the manner of sustain release and inhibit the inflammation persistently. It is expected to reveal the question whether the inflammation is the potentional target to inhibit the residual tumors to find a new mechanism for the residual tumor cell invasion and metastasis after the embolization.

经导管动脉化疗栓塞术是治疗不可切除肝癌的主要方法，栓塞后残存肿瘤细胞成为肝癌复发和转移的重要来源，如何抑制残存肿瘤细胞是亟待解决的难题。肝癌栓塞治疗后残存癌组织内及癌周组织浸润大量炎性细胞，而炎症反应促进了肿瘤的发生与进展。据此我们推测肝癌栓塞治疗后局部的炎症反应是残存癌细胞生存的重要因素，并以此为依据进行了预实验，发现栓塞后残存癌组织及癌周组织内的浸润炎症参与了残存癌组织新生血管生成，中性粒细胞可能起到了关键作用，但是其具体机制尚有待探索。因此我们拟通过兔VX2种植性肝癌模型，采用缓释的载地塞米松磷酸钠DC Bead药物洗脱微球，持续抑制肝癌栓塞后残存癌组织及癌周的炎症反应，研究栓塞后炎症反应与残存肿瘤组织新生血管生成、细胞增殖及代谢等的关系，以阐明栓塞后诱发的炎症反应是否可以成为抑制残存肿瘤细胞生存的新靶点，藉此发现肝癌化疗栓塞后残存肿瘤细胞侵袭与转移的新机制。

经导管动脉化疗栓塞术是治疗不可切除肝癌的主要方法，栓塞后残存肿瘤细胞成为肝癌复发和转移的重要来源，如何抑制残存肿瘤细胞是亟待解决的难题。肝癌栓塞治疗后残存癌组织内及癌周组织浸润大量炎性细胞，而炎症反应促进了肿瘤的发生与进展。据此我们推测肝癌栓塞治疗后局部的炎症反应是残存癌细胞生存的重要因素，并以此为依据进行了预实验，发现栓塞后残存癌组织及癌周组织内的浸润炎症参与了残存癌组织新生血管生成，中性粒细胞可能起到了关键作用，但是其具体机制尚有待探索。因此我们拟通过兔VX2种植性肝癌模型，采用缓释的载地塞米松磷酸钠DC Bead药物洗脱微球，持续抑制肝癌栓塞后残存癌组织及癌周的炎症反应，研究栓塞后炎症反应与残存肿瘤组织新生血管生成、细胞增殖及代谢等的关系，以阐明栓塞后诱发的炎症反应是否可以成为抑制残存肿瘤细胞生存的新靶点，藉此发现肝癌化疗栓塞后残存肿瘤细胞侵袭与转移的新机制。