医学信息
醫學信息
의학신식
MEDICAL INFORMATION
2014年
9期
224-225
,共2页
姚懿雯%吴军录%权文强%万海英%李冬
姚懿雯%吳軍錄%權文彊%萬海英%李鼕
요의문%오군록%권문강%만해영%리동
尿多酸肽%肺癌%肿瘤生长%生存期%增殖%凋亡
尿多痠肽%肺癌%腫瘤生長%生存期%增殖%凋亡
뇨다산태%폐암%종류생장%생존기%증식%조망
CDA-2%Lung cancer%Tumor growth%Life span%Proliferation%Apoptosis
目的:研究尿多酸肽(CDA-2)作用于转移性肺肿瘤小鼠的机制。方法通过注射鼠Lewis 肺癌细胞到C57BL/6小鼠体内建立小鼠转移性肺癌模型。采用HE染色对小鼠肺部肿瘤数、肿瘤大小进行评价。利用Kaplan-Meier (K-M)生存率曲线分析小鼠生存情况。免疫组化方法检测小鼠肿瘤增殖抗原 Ki-67的表达;TUNEL凋亡免疫组化染色观察肿瘤细胞的凋亡。结果经CDA-2治疗后,小鼠的肺肿瘤数和最大肿瘤尺寸均显著低于 PBS组肿瘤小鼠,并且CDA-2呈剂量依赖性抑制肿瘤的生长(均P<0.05)。K-M结果显示,使用PBS组肿瘤小鼠的生存时间显著低于CDA-2治疗组,且随着CDA-2剂量增加肿瘤小鼠生存时间不断延长。免疫组化染色结果显示,肺肿瘤小鼠经CDA-2治疗后,Ki-67阳性肿瘤细胞数显著低于PBS治疗的肿瘤小鼠(P<0.05);而肿瘤凋亡细胞数却明显高于 PBS组(P<0.001)。结论 CDA-2可抑制小鼠肺癌的生长;延长肺癌小鼠的生存期;抑制肿瘤细胞增殖及诱导肿瘤细胞凋亡。
目的:研究尿多痠肽(CDA-2)作用于轉移性肺腫瘤小鼠的機製。方法通過註射鼠Lewis 肺癌細胞到C57BL/6小鼠體內建立小鼠轉移性肺癌模型。採用HE染色對小鼠肺部腫瘤數、腫瘤大小進行評價。利用Kaplan-Meier (K-M)生存率麯線分析小鼠生存情況。免疫組化方法檢測小鼠腫瘤增殖抗原 Ki-67的錶達;TUNEL凋亡免疫組化染色觀察腫瘤細胞的凋亡。結果經CDA-2治療後,小鼠的肺腫瘤數和最大腫瘤呎吋均顯著低于 PBS組腫瘤小鼠,併且CDA-2呈劑量依賴性抑製腫瘤的生長(均P<0.05)。K-M結果顯示,使用PBS組腫瘤小鼠的生存時間顯著低于CDA-2治療組,且隨著CDA-2劑量增加腫瘤小鼠生存時間不斷延長。免疫組化染色結果顯示,肺腫瘤小鼠經CDA-2治療後,Ki-67暘性腫瘤細胞數顯著低于PBS治療的腫瘤小鼠(P<0.05);而腫瘤凋亡細胞數卻明顯高于 PBS組(P<0.001)。結論 CDA-2可抑製小鼠肺癌的生長;延長肺癌小鼠的生存期;抑製腫瘤細胞增殖及誘導腫瘤細胞凋亡。
목적:연구뇨다산태(CDA-2)작용우전이성폐종류소서적궤제。방법통과주사서Lewis 폐암세포도C57BL/6소서체내건립소서전이성폐암모형。채용HE염색대소서폐부종류수、종류대소진행평개。이용Kaplan-Meier (K-M)생존솔곡선분석소서생존정황。면역조화방법검측소서종류증식항원 Ki-67적표체;TUNEL조망면역조화염색관찰종류세포적조망。결과경CDA-2치료후,소서적폐종류수화최대종류척촌균현저저우 PBS조종류소서,병차CDA-2정제량의뢰성억제종류적생장(균P<0.05)。K-M결과현시,사용PBS조종류소서적생존시간현저저우CDA-2치료조,차수착CDA-2제량증가종류소서생존시간불단연장。면역조화염색결과현시,폐종류소서경CDA-2치료후,Ki-67양성종류세포수현저저우PBS치료적종류소서(P<0.05);이종류조망세포수각명현고우 PBS조(P<0.001)。결론 CDA-2가억제소서폐암적생장;연장폐암소서적생존기;억제종류세포증식급유도종류세포조망。
Objective The aim of the study was to investigate the ef ect of CDA-2 on lung tumor in mice tumor models. Methods C57BL/6 mice were used to establish a lung cancer model by intravenous injection of LLC cells. Tumorigenesis was evaluated by tumor multiplicity and maximal tumor sizes. Kaplan Meier (K-M) survival curve was used to analyze survival rate of mice. The expression of Ki-67 in the tumor tissue was measured by immunohistochemical analysis. The apoptosis of tumor cells was analyzed by TUNEL staining. Results Lung tumor mice treated with CDA-2 significantly decreased lung tumor multiplicity and maximal tumor sizes compared to PBS group and depended on CDA-2 does inhibition(P<0.05). K-M survival analysis showed CDA-2-treated tumor mice significant prolonged the life time compared to PBS-treated mice. The numbers of Ki-67-positive tumor cells were significant lower in CDA-2-treated tumor mice than PBS-treated mice (P<0.05); In contrast, lung tumor cells showed significant rate of apoptosis and death when CDA-2 treatment (P<0.001). Conclusions CDA-2 inhibited lung tumor growth in mice;prolonging the life span of lung tumor mice;inhibiting tumor cells proliferation and inducing tumor cells apoptosis.