中华放射医学与防护杂志
中華放射醫學與防護雜誌
중화방사의학여방호잡지
Chinese Journal of Radiological Medicine and Protection
2014年
1期
26-29,33
,共5页
刘敬佳%王皓%曲昂%李金娜%赵勇%王俊杰
劉敬佳%王皓%麯昂%李金娜%趙勇%王俊傑
류경가%왕호%곡앙%리금나%조용%왕준걸
C225%持续低剂量率照射%放射敏感性%结直肠癌细胞%细胞凋亡
C225%持續低劑量率照射%放射敏感性%結直腸癌細胞%細胞凋亡
C225%지속저제량솔조사%방사민감성%결직장암세포%세포조망
C225%Continuous low dose rate radiation%Radiosensitization%Colorectal cancer cell%Cell apoptosis
目的 探讨在125I放射性粒子持续低剂量率照射下,西妥昔单抗对结直肠癌细胞CL187放射敏感性的影响及可能的机制.方法 实验将直肠癌细胞CL187分为空白对照组、单纯100 nmol/L C225处理组、单纯125I-CLDR照射组和C225联合125I-CLDR组.克隆形成实验检测C225是否影响人结直肠癌CL187细胞对125I放射性粒子持续低剂量率照射的放射敏感性.流式细胞仪检测C225对125I-CLDR照射诱导的细胞凋亡的影响.细胞周期检测C225对细胞周期的调节.瑞氏姬姆萨染色检测有丝分裂指数.Western blot检测细胞内Bax、Bcl-2的水平.结果 100 nmol/LC225的放射增敏比为1.4,并能够增加125I-CLDR照射诱导的细胞凋亡(=6.6,P＜0.05),增加Bax/Bcl-2比值.与空白对照组相比,单独C225处理可使CL187细胞G1期阻滞(t=3.0,P＜0.05),单纯125I-CLDR照射组细胞也存在G1期阻滞(t=8.5,P＜0.01),两者联合时的G1期阻滞效应与125I-CLDR单独处理时相比,差异无统计学意义(t=0.8,P＞0.05).有丝分裂指数检测结果显示,各实验组与对照组相比差异无统计学意义.结论 C225可增加结直肠癌细胞CL187对125I-CLDR照射的放射敏感性,机制可能是C225增加细胞内Bax/Bcl-2比值,增加125I-CLDR诱导的细胞凋亡,与细胞周期阻滞和细胞周期检查点功能无关.
目的 探討在125I放射性粒子持續低劑量率照射下,西妥昔單抗對結直腸癌細胞CL187放射敏感性的影響及可能的機製.方法 實驗將直腸癌細胞CL187分為空白對照組、單純100 nmol/L C225處理組、單純125I-CLDR照射組和C225聯閤125I-CLDR組.剋隆形成實驗檢測C225是否影響人結直腸癌CL187細胞對125I放射性粒子持續低劑量率照射的放射敏感性.流式細胞儀檢測C225對125I-CLDR照射誘導的細胞凋亡的影響.細胞週期檢測C225對細胞週期的調節.瑞氏姬姆薩染色檢測有絲分裂指數.Western blot檢測細胞內Bax、Bcl-2的水平.結果 100 nmol/LC225的放射增敏比為1.4,併能夠增加125I-CLDR照射誘導的細胞凋亡(=6.6,P＜0.05),增加Bax/Bcl-2比值.與空白對照組相比,單獨C225處理可使CL187細胞G1期阻滯(t=3.0,P＜0.05),單純125I-CLDR照射組細胞也存在G1期阻滯(t=8.5,P＜0.01),兩者聯閤時的G1期阻滯效應與125I-CLDR單獨處理時相比,差異無統計學意義(t=0.8,P＞0.05).有絲分裂指數檢測結果顯示,各實驗組與對照組相比差異無統計學意義.結論 C225可增加結直腸癌細胞CL187對125I-CLDR照射的放射敏感性,機製可能是C225增加細胞內Bax/Bcl-2比值,增加125I-CLDR誘導的細胞凋亡,與細胞週期阻滯和細胞週期檢查點功能無關.
목적 탐토재125I방사성입자지속저제량솔조사하,서타석단항대결직장암세포CL187방사민감성적영향급가능적궤제.방법 실험장직장암세포CL187분위공백대조조、단순100 nmol/L C225처리조、단순125I-CLDR조사조화C225연합125I-CLDR조.극륭형성실험검측C225시부영향인결직장암CL187세포대125I방사성입자지속저제량솔조사적방사민감성.류식세포의검측C225대125I-CLDR조사유도적세포조망적영향.세포주기검측C225대세포주기적조절.서씨희모살염색검측유사분렬지수.Western blot검측세포내Bax、Bcl-2적수평.결과 100 nmol/LC225적방사증민비위1.4,병능구증가125I-CLDR조사유도적세포조망(=6.6,P＜0.05),증가Bax/Bcl-2비치.여공백대조조상비,단독C225처리가사CL187세포G1기조체(t=3.0,P＜0.05),단순125I-CLDR조사조세포야존재G1기조체(t=8.5,P＜0.01),량자연합시적G1기조체효응여125I-CLDR단독처리시상비,차이무통계학의의(t=0.8,P＞0.05).유사분렬지수검측결과현시,각실험조여대조조상비차이무통계학의의.결론 C225가증가결직장암세포CL187대125I-CLDR조사적방사민감성,궤제가능시C225증가세포내Bax/Bcl-2비치,증가125I-CLDR유도적세포조망,여세포주기조체화세포주기검사점공능무관.
Objective To investigate the effect of cetuximab (C225) on the radiosensitivity of colorectal cancer cells CL187 and underlying mechanism.Methods Cell survival was detected by colony forming assay.The levels of apoptosis and cell cycle distribution were determined by flow cytometer.The mitotic ratio was measured by Wright' s-Giemsa mixed coloring method.The protein levels of Bax and Bcl2 were detected by Western blot.Results The sensitizing enhancement ratio of C225 was approximately 1.4.C225 treatment and 125I seed radiation induced G1 cell cycle arrest individually.C225 increased the radiation-induced apoptosis (t =6.6,P ＜ 0.05) and cellular Bax/Bcl-2 ratio (t =9.4,P ＜ 0.05),but did not increase radiation-induced G1 arrest.In addition,there was no difference in mitotic index among different groups.Conclusions C225 sensitizes CL187 to 125I seed irradiation,which might be related with increase of radiation-induced apoptosis.
