雙歧桿菌介導(dǎo)CTP-NPRL2對裸鼠腎癌生長及凋亡的影響
發(fā)布時間:2018-04-25 13:11
本文選題:腎腫瘤 + 雙歧桿菌; 參考:《重慶醫(yī)學》2017年18期
【摘要】:目的探討雙歧桿菌介導(dǎo)CTP-NPRL2對裸鼠腎癌生長及凋亡的影響。方法構(gòu)建pET15b-CTP-NPRL2并電轉(zhuǎn)雙歧桿菌,Western blot驗證蛋白表達。采用腎癌細胞懸液皮下注射法建立裸鼠腎癌模型,并分為觀察組與對照組(每組8只),分別經(jīng)尾靜脈注射攜帶pET15b-CTP-NPRL2的雙歧桿菌與生理鹽水,每周1次,4周后處死裸鼠,稱取裸鼠及荷瘤質(zhì)量,TUNEL法檢測腎癌組織凋亡。結(jié)果觀察組與對照組裸鼠質(zhì)量分別為(26.24±1.98)g、(23.28±2.17)g,荷瘤質(zhì)量分別為(1.37±0.12)g、(1.68±0.18)g,兩組比較差異均有統(tǒng)計學意義(P0.05)。TUNEL檢測顯示觀察組凋亡指數(shù)(23.27±5.14)%明顯高于對照組(10.37±2.58)%,兩組比較差異有統(tǒng)計學意義(P0.05)。結(jié)論雙歧桿菌介導(dǎo)CTP-NPRL2對裸鼠腎癌生長具有抑制功能,并明顯增加了腎癌細胞的凋亡。
[Abstract]:Objective to explore the effect of bifidobacteria mediated CTP-NPRL2 on the growth and apoptosis of nude mice kidney cancer. Methods to construct pET15b-CTP-NPRL2 and convert Bifidobacterium and Western blot to verify protein expression. The renal carcinoma model of nude mice was established by subcutaneous injection of renal cell suspension, and divided into the observation group and the control group (8 rats in each group), and the pE was injected into the tail vein to carry pE respectively. T15b-CTP-NPRL2 of Bifidobacterium and saline, 1 times a week, 4 weeks after the death of nude mice, called nude mice and tumor bearing mass, TUNEL method to detect the apoptosis of renal carcinoma tissue, the results of the observation group and the control group were (26.24 + 1.98) g, (23.28 + 2.17) g, the mass of the tumor was (1.37 + 0.12) g, (1.68 + 0.18) g, and the difference of the two groups was statistically significant P0.05.TUNEL detection showed that the apoptotic index (23.27 + 5.14)% of the observation group was significantly higher than that of the control group (10.37 + 2.58)%, and the two groups had a significant difference (P0.05). Conclusion Bifidobacterium mediated CTP-NPRL2 inhibited the growth of nude mice and increased the apoptosis of renal cell carcinoma cells.
【作者單位】: 重慶市永榮礦業(yè)有限公司總醫(yī)院泌尿外科;重慶醫(yī)科大學附屬第一醫(yī)院泌尿外科;
【基金】:重慶市衛(wèi)生局面上項目(2013-2-262)
【分類號】:R737.11
,
本文編號:1801471
本文鏈接:http://sikaile.net/yixuelunwen/mjlw/1801471.html
最近更新
教材專著