CAJ | 학술논문

目的研究内皮抑素对小鼠Lewis肺癌生长、淋巴管生成和淋巴结转移的影响.方法用40只小鼠建立Lewis肺癌模型,然后分为两组,分别注射生理盐水(对照组)和重组内皮抑素endostar(治疗组).记录并比较两组肺表面肿瘤数、肿瘤大小及淋巴结转移率,免疫组化法检测肿瘤微淋巴管密度和血管内皮生长因子-C(VEGF-C)表达,分析内皮抑素对肿瘤微淋巴管密度(MLVD)和VEGF-C表达的影响.结果治疗组肺表面肿瘤数、肿瘤平均长径均低于治疗组,差异有统计学意义(P＜0.05).对照组和治疗组MLVD分别为7.8±1.6、5.7±1. 6,两组分别有8例和2例见淋巴结转移,差异均有统计学意义(P＜0.05).对照组VEGF-C表达阳性率为66.7%(12/18),治疗组为27.8%(5/18),差异有统计学意义(P＜0.05).结论内皮抑素对小鼠肺癌生长、淋巴管生成和淋巴结转移有抑制作用,这种抑制作用可能与内皮抑素对VEGF-C表达的调控有关.
목적 연구내피억소대소서Lewis폐암생장、림파관생성화림파결전이적영향.방법 용40지소서건립Lewis폐암모형,연후분위량조,분별주사생리염수(대조조)화중조내피억소endostar(치료조).기록병비교량조폐표면종류수、종류대소급림파결전이솔,면역조화법검측종류미림파관밀도화혈관내피생장인자-C(VEGF-C)표체,분석내피억소대종류미림파관밀도(MLVD)화VEGF-C표체적영향.결과 치료조폐표면종류수、종류평균장경균저우치료조,차이유통계학의의(P＜0.05).대조조화치료조MLVD분별위7.8±1.6、5.7±1. 6,량조분별유8례화2례견림파결전이,차이균유통계학의의(P＜0.05).대조조VEGF-C표체양성솔위66.7%(12/18),치료조위27.8%(5/18),차이유통계학의의(P＜0.05).결론 내피억소대소서폐암생장、림파관생성화림파결전이유억제작용,저충억제작용가능여내피억소대VEGF-C표체적조공유관.
Objective To investigate the effects of endostar, a recombined humanized endostatin,on the growth, lymphangiogenesis and lymphatic metastasis of Lewis lung carcinoma xenograft in mice. Methods Lewis lung carcinoma (LLC) xenograft were established in C57 mice by intravenious transplantation of 1 × 106 cells. Then tumor-bearing mice were assigned into two groups: control group received caudal vein injections of 0. 2 ml of 0. 9% sodium chloride for 15 days, and treatment group received 500 μg endostar daily. Six weeks after LLC cell injection mice were sacrificed, and then tumor numbers and size were recorded. The expression of vascular endothelial growth factor-c (VEGF-C) and microlymphatic vessel density( MLVD)were observed by immunohistochemical staining. Results Tumor number and size of control group were significantly higher than those of treatment group. The microlymphatic vessel density (MLVD) was 5.7 ± 1.6 in the treatment group, which was markedly lower than in the control mice (7. 8 ±1.6). Two lymph node metastases were observed in treatment group, and eight in control group. Lymphatic metastases were more frequent in control group than in treatment group. Expression of VEGF-C in control group was significantly higher than that in treatment group. Conclusion Endostar significantly inhibits the growth, lymphangiogenesis and lymphatic metastasis of Lewis lung carcinoma xenografts, and the inhibitory effect is due to its ability to regulate the expression of VEGF-C of tumors in part.