CAJ | 학술논문

目的：观察恩度联合放疗对Lewis肺癌的生长抑制作用，检测肿瘤中微血管密度（ MVD）及αvβ3 mRNA的表达，探讨其在肿瘤血管“正常化”及协同抑瘤作用中的可能机制。方法荷瘤小鼠随机分成4组：空白对照组（NC），恩度组（ES），放射治疗组（RT），恩度联合放疗组（ES＋RT）。从开始治疗后隔日测量肿瘤体积，绘制生长曲线。免疫组化法及RT-PCR分别检测各组肿瘤组织中MVD及αvβ3 mR-NA的表达情况。结果（1）ES＋RT组的抑瘤作用最为明显；（2）与空白对照组相比，RT组随时间延长微血管计数逐渐增加，ES组及ES＋RT组下降，其中ES＋RT组比ES组下降更为明显，差异有统计学意义（P＜0．05）；（3）与空白对照组相比，RT组αvβ3 mRNA表达水平升高，而ES及ES＋RT组则降低，ES＋RT组降低更为明显，ES组在第6天扩增倍数最低，各治疗组在d8～d12均有统计学差异（ P＜0．05）。结论恩度联合放疗显著抑制Lewis肿瘤的生长；恩度能使肿瘤MVD明显减少，形态趋于正常；恩度可下调αvβ3 mRNA的表达，改善肿瘤组织紊乱的血管网，降低乏氧，可能是放疗增敏的机制之一。
목적：관찰은도연합방료대Lewis폐암적생장억제작용，검측종류중미혈관밀도（ MVD）급αvβ3 mRNA적표체，탐토기재종류혈관“정상화”급협동억류작용중적가능궤제。방법하류소서수궤분성4조：공백대조조（NC），은도조（ES），방사치료조（RT），은도연합방료조（ES＋RT）。종개시치료후격일측량종류체적，회제생장곡선。면역조화법급RT-PCR분별검측각조종류조직중MVD급αvβ3 mR-NA적표체정황。결과（1）ES＋RT조적억류작용최위명현；（2）여공백대조조상비，RT조수시간연장미혈관계수축점증가，ES조급ES＋RT조하강，기중ES＋RT조비ES조하강경위명현，차이유통계학의의（P＜0．05）；（3）여공백대조조상비，RT조αvβ3 mRNA표체수평승고，이ES급ES＋RT조칙강저，ES＋RT조강저경위명현，ES조재제6천확증배수최저，각치료조재d8～d12균유통계학차이（ P＜0．05）。결론은도연합방료현저억제Lewis종류적생장；은도능사종류MVD명현감소，형태추우정상；은도가하조αvβ3 mRNA적표체，개선종류조직문란적혈관망，강저핍양，가능시방료증민적궤제지일。
Objective To observe the MVD and integrin αvβ3 mRNA expression changes in tumor -bearing rats by using endostar combined with radiotherapy ,and to explore the potential synergy mechanism .Meth-ods We randomly divided the tumor -bearing rats into four groups:control group(NC),endostar group(ES), radiation treatment group ( RT) and endostar combined radiotherapy group ( ES +RT) .Tumor inhibition rate was calculated every other day .Microvessel density and αvβ3mRNA were texted by immunohistochemical or real time PCR in each group.Results (1)ES+RT group showed the most obvious inhibition rate;(2)Compared with NC group,microvessel density of RT was increased ,but decreased in ES group and ES +RT group significantly ( P<0.05);(3)Compared with NC group,αvβ3 mRNA expression of RT group was increased,while decreased in ES group and ES+RT group,and ES +RT group displayed a greater decrease when compared to ES group ( P<0.05).Conclusion Endostar combined radiotherapy can inhibit the growth of cancer and the expression ofαvβ3mRNA,improve the disorders of tumor vascular network .It may be one of the mechanisms of increasing radi-osensitization.