华中科技大学学报(医学版)
華中科技大學學報(醫學版)
화중과기대학학보(의학판)
ACTA UNIVERSITATIS MEDICINAE TONGJI
2014年
2期
148-152,157
,共6页
毕建平%马虹%张涛%张盛%李勤
畢建平%馬虹%張濤%張盛%李勤
필건평%마홍%장도%장성%리근
表皮生长因子%盐酸埃克替尼%放疗%放射敏感性%DNA双键断裂修复
錶皮生長因子%鹽痠埃剋替尼%放療%放射敏感性%DNA雙鍵斷裂脩複
표피생장인자%염산애극체니%방료%방사민감성%DNA쌍건단렬수복
epidermal grow th factor%icotinib hydrochloride%radiotherapy%radiosensitivity%double-strand break repair
目的:研究盐酸埃克替尼联合放疗抗肿瘤的效果及机制。方法建立裸鼠人大肠腺癌HT29细胞株荷瘤模型,随机分为4组:对照组、盐酸埃克替尼组、放疗组、联合治疗组,用免疫荧光方法检测肿瘤组织γ-H2AX、53BP1表达,及细胞增殖相关抗原Ki-67和凋亡相关抗原Caspase-3的表达,并计算组织细胞内γ-H2AX、53BP1荧光焦点平均值以及肿瘤增殖率和肿瘤凋亡数。结果盐酸埃克替尼联合放疗组较其他3组显著增加肿瘤组织γ-H2AX和53BP1的表达,抑制肿瘤细胞增殖(Ki-67阳性细胞率降低)和增加肿瘤细胞凋亡(Caspase-3阳性细胞数增加)(均P<0.01)。结论盐酸埃克替尼与放疗同步显著加重肿瘤细胞内的DNA损伤,抑制肿瘤增殖,增加肿瘤凋亡,从而增进放疗疗效。
目的:研究鹽痠埃剋替尼聯閤放療抗腫瘤的效果及機製。方法建立裸鼠人大腸腺癌HT29細胞株荷瘤模型,隨機分為4組:對照組、鹽痠埃剋替尼組、放療組、聯閤治療組,用免疫熒光方法檢測腫瘤組織γ-H2AX、53BP1錶達,及細胞增殖相關抗原Ki-67和凋亡相關抗原Caspase-3的錶達,併計算組織細胞內γ-H2AX、53BP1熒光焦點平均值以及腫瘤增殖率和腫瘤凋亡數。結果鹽痠埃剋替尼聯閤放療組較其他3組顯著增加腫瘤組織γ-H2AX和53BP1的錶達,抑製腫瘤細胞增殖(Ki-67暘性細胞率降低)和增加腫瘤細胞凋亡(Caspase-3暘性細胞數增加)(均P<0.01)。結論鹽痠埃剋替尼與放療同步顯著加重腫瘤細胞內的DNA損傷,抑製腫瘤增殖,增加腫瘤凋亡,從而增進放療療效。
목적:연구염산애극체니연합방료항종류적효과급궤제。방법건립라서인대장선암HT29세포주하류모형,수궤분위4조:대조조、염산애극체니조、방료조、연합치료조,용면역형광방법검측종류조직γ-H2AX、53BP1표체,급세포증식상관항원Ki-67화조망상관항원Caspase-3적표체,병계산조직세포내γ-H2AX、53BP1형광초점평균치이급종류증식솔화종류조망수。결과염산애극체니연합방료조교기타3조현저증가종류조직γ-H2AX화53BP1적표체,억제종류세포증식(Ki-67양성세포솔강저)화증가종류세포조망(Caspase-3양성세포수증가)(균P<0.01)。결론염산애극체니여방료동보현저가중종류세포내적DNA손상,억제종류증식,증가종류조망,종이증진방료료효。
Objective To examine the antitumor efficacy of a combination of icotinib hydrochloride and radiotherapy in a human tumor xenograft model.Methods Tumor-bearing nude mouse models were established by using HT29 cells (a human colorectal adenocarcinoma cell line ).Four groups were set up in terms of different treatments (administration of icotinib hydro-chloride or irradiation ):control group ,icotinib hydrochloride group ;radiotherapy (RT ) group;icotinib hydrochloride + RT group.The expressions of γ-H2AX ,53BP1 Ki-67 and Caspase-3 were detected by immunofluorescence.The average fluorescent values of γ-H2AX and 53BP1 were obtained ,and the proliferation rate of tumor cells and the number of apoptotic cells calculat-ed.Results Icotinib hydrochloride combined with RT significantly inhibited the DNA repair by increasing the expression of γ-H2AX and 53BP1 and the treatment could inhibit the proliferation and increase the apoptosis of tumor tissue ( P< 0.01 ) . Conclusion Icotinib hydrochloride combined with RT enhances the radiosensitivity of tumor cells by aggravating the DNA inju-ry ,inhibiting the proliferation and increasing apoptosis of tumor cells.