临床误诊误治
臨床誤診誤治
림상오진오치
CLINICAL MISDIAGNOSIS & MISTHERAPY
2014年
12期
105-108
,共4页
小鼠%肺肿瘤%原癌基因蛋白质c-bcl-2%血管内皮生长因子类%果王素
小鼠%肺腫瘤%原癌基因蛋白質c-bcl-2%血管內皮生長因子類%果王素
소서%폐종류%원암기인단백질c-bcl-2%혈관내피생장인자류%과왕소
Mice%Lung cancer%Proto-oncogene proteins c-bcl-2%Survivin%VEGF%Kiwi essence
目的：观察果王素对肺腺癌小鼠移植瘤生长的抑制作用,并探讨其作用机制。方法接种Lewis肺腺癌细胞构建肺腺癌小鼠移植瘤模型,将40只接种Lewis肺腺癌细胞的C57BL/6J小鼠随机分为对照组(予0.9%氯化钠注射液)、果王素组(予果王素180 mg/kg )、化疗组(予顺铂联合吉西他滨)、低剂量果王素并化疗组(予果王素60 mg/kg联合顺铂、吉西他滨)、高剂量果王素并化疗组(予果王素180 mg/kg联合顺铂、吉西他滨),每组各8只。肿瘤细胞接种4 d成瘤后予相应的药物干预,接种20 d后处死小鼠,剥离皮下肿瘤。应用免疫组织化学法检测移植瘤组织中血管内皮生长因子(VEGF)、Survivin和B细胞淋巴瘤/白血病-2(Bcl-2)的表达水平。结果各药物干预组肿瘤的生长均受到抑制,果王素组、化疗组、低剂量果王素并化疗组、高剂量果王素并化疗组抑瘤率分别为14.95%、41．77%、44.21%、59.68%,组间比较差异均有统计学意义(P<0．05,P<0．01)。各药物干预组VEGF、Survivin、Bcl-2表达均较对照组低,差异均有统计学意义(P<0．05,P<0．01)。结论果王素能抑制小鼠Lewis肺腺癌的生长,且果王素与顺铂、吉西他滨联用的抗肿瘤作用更明显,可能是通过抑制微血管形成及Survivin、Bcl-2表达发挥作用。
目的：觀察果王素對肺腺癌小鼠移植瘤生長的抑製作用,併探討其作用機製。方法接種Lewis肺腺癌細胞構建肺腺癌小鼠移植瘤模型,將40隻接種Lewis肺腺癌細胞的C57BL/6J小鼠隨機分為對照組(予0.9%氯化鈉註射液)、果王素組(予果王素180 mg/kg )、化療組(予順鉑聯閤吉西他濱)、低劑量果王素併化療組(予果王素60 mg/kg聯閤順鉑、吉西他濱)、高劑量果王素併化療組(予果王素180 mg/kg聯閤順鉑、吉西他濱),每組各8隻。腫瘤細胞接種4 d成瘤後予相應的藥物榦預,接種20 d後處死小鼠,剝離皮下腫瘤。應用免疫組織化學法檢測移植瘤組織中血管內皮生長因子(VEGF)、Survivin和B細胞淋巴瘤/白血病-2(Bcl-2)的錶達水平。結果各藥物榦預組腫瘤的生長均受到抑製,果王素組、化療組、低劑量果王素併化療組、高劑量果王素併化療組抑瘤率分彆為14.95%、41．77%、44.21%、59.68%,組間比較差異均有統計學意義(P<0．05,P<0．01)。各藥物榦預組VEGF、Survivin、Bcl-2錶達均較對照組低,差異均有統計學意義(P<0．05,P<0．01)。結論果王素能抑製小鼠Lewis肺腺癌的生長,且果王素與順鉑、吉西他濱聯用的抗腫瘤作用更明顯,可能是通過抑製微血管形成及Survivin、Bcl-2錶達髮揮作用。
목적：관찰과왕소대폐선암소서이식류생장적억제작용,병탐토기작용궤제。방법접충Lewis폐선암세포구건폐선암소서이식류모형,장40지접충Lewis폐선암세포적C57BL/6J소서수궤분위대조조(여0.9%록화납주사액)、과왕소조(여과왕소180 mg/kg )、화료조(여순박연합길서타빈)、저제량과왕소병화료조(여과왕소60 mg/kg연합순박、길서타빈)、고제량과왕소병화료조(여과왕소180 mg/kg연합순박、길서타빈),매조각8지。종류세포접충4 d성류후여상응적약물간예,접충20 d후처사소서,박리피하종류。응용면역조직화학법검측이식류조직중혈관내피생장인자(VEGF)、Survivin화B세포림파류/백혈병-2(Bcl-2)적표체수평。결과각약물간예조종류적생장균수도억제,과왕소조、화료조、저제량과왕소병화료조、고제량과왕소병화료조억류솔분별위14.95%、41．77%、44.21%、59.68%,조간비교차이균유통계학의의(P<0．05,P<0．01)。각약물간예조VEGF、Survivin、Bcl-2표체균교대조조저,차이균유통계학의의(P<0．05,P<0．01)。결론과왕소능억제소서Lewis폐선암적생장,차과왕소여순박、길서타빈련용적항종류작용경명현,가능시통과억제미혈관형성급Survivin、Bcl-2표체발휘작용。
Objective To observe the inhibitory effect of Kiwi essence on xenograft growth of lung adenocarcinoma in mice. Methods Forty C57BL/6J mice bearing Lewis cells were randomized into five groups: control group (0. 9% sodium chloride) , Kiwi essence group ( Kiwi essence 180 mg/kg) , chemotherapy group ( cisplatin and gemcitabine) , low-dose Kiwi essence combined chemotherapy group ( Kiwi essence 60 mg/kg combined cisplatin and gemcitabine) , high-dose Kiwi essence combined chemotherapy group (180 mg/kg Kiwi essence combined cisplatin and gemcitabine). 4 days after being inoculated with adenocarcinoma cells, drug intervention was given in five groups of mice. Mice were sacrificed at day 20 after tumor inoc-ulation. The subcutaneous tumors were stripped for histological examination. The tumor inhibitory rate was measured. The ex-pressions of vascular endothelial growth factor ( VEGF) , Bcl-2 and Survivin were determined by immunohistochemistry method with image analyzing system. Results There were significantly lower values in subcutaneous tumor volume and weight in drug-treated groups. The inhibitory rate was 14. 95%, 41. 77%, 44. 21% and 59. 68% in Kiwi essence group, chemotherapy group, low-dose Kiwi essence combined chemotherapy group, high-dose Kiwi essence combined chemotherapy group respec-tively (P<0. 05, P<0. 01). VEGF, Survivin, Bcl-2 in each group were lower than in the control group (P<0. 05, P<0. 01). Conclusion Kiwi essence can produce a synergetic inhibitory activity against tumor growth of lung adenocarcinoma and enhance GP therapeutic regimen ( cisplatin plus gemcitabine) to inhibit tumor growth of lung adenocarcinoma, which may be associated with the effect of suppressing the expression of angiogenesis, Survivin and Bcl-2.
