CAJ | 학술논문

目的：探讨纳米脂质体槲皮素（nLQ）诱导人食管癌Eca-9706细胞逆转化及凋亡的效应及其机制。方法：采用旋转蒸发法制备以氯仿和DMSO为溶剂的脂质体槲皮素,将其超声波破碎并经80nm滤膜过滤制成nLQ,不同浓度（10、20、40、80和100μmol/L）作用于Eca-9706细胞,用MTT法检测各组Eca-9706细胞的生长抑制率。分别取Eca-9706细胞,分为nLQ组（加40μmol/LnLQ）和对照组。TUNEL法检测2组细胞凋亡率;免疫细胞化学/免疫印迹法检测2组处理48h后Eca-9706细胞CyclinD1、PTEN、c-Met、VEGF、组蛋白去乙酰化酶（HDAC）1及NF-κB表达的变化。结果：各组Eca-9706细胞生长抑制率（F分别为128.041、142.683和231.054,P〈0.001）和2组细胞凋亡率（t=94.770,P〈0.001）比较,差异均有统计学意义。PTEN免疫反应性和印记信号增强（t分别为5.352和4.308,P均〈0.05）,Cyclin D1、c-Met、VEGF、HDAC1和NF-κB的免疫反应性减弱（t分别为4.006、9.184、13.853、4.698和3.575,P均〈0.05）,其印迹信号亦减弱（t分别为3.827、6.399、7.868、4.695和3.406,P均〈0.05）;以上各细胞蛋白的免疫细胞和免疫印迹信号之间呈正相关（rs分别为0.952、0.915、0.927、0.842、0.879和0.855,P均〈0.05）。结论：nLQ可抑制Eca-9706细胞生长及增殖,逆转Eca-9706细胞PTEN的低表达和c-Met及VEGF的高表达,并通过抑制HDAC1和NF-κB及激活PTEN表达的HDAC抑制信号途径而诱导细胞凋亡。
목적：탐토납미지질체곡피소（nLQ）유도인식관암Eca-9706세포역전화급조망적효응급기궤제。방법：채용선전증발법제비이록방화DMSO위용제적지질체곡피소,장기초성파파쇄병경80nm려막과려제성nLQ,불동농도（10、20、40、80화100μmol/L）작용우Eca-9706세포,용MTT법검측각조Eca-9706세포적생장억제솔。분별취Eca-9706세포,분위nLQ조（가40μmol/LnLQ）화대조조。TUNEL법검측2조세포조망솔;면역세포화학/면역인적법검측2조처리48h후Eca-9706세포CyclinD1、PTEN、c-Met、VEGF、조단백거을선화매（HDAC）1급NF-κB표체적변화。결과：각조Eca-9706세포생장억제솔（F분별위128.041、142.683화231.054,P〈0.001）화2조세포조망솔（t=94.770,P〈0.001）비교,차이균유통계학의의。PTEN면역반응성화인기신호증강（t분별위5.352화4.308,P균〈0.05）,Cyclin D1、c-Met、VEGF、HDAC1화NF-κB적면역반응성감약（t분별위4.006、9.184、13.853、4.698화3.575,P균〈0.05）,기인적신호역감약（t분별위3.827、6.399、7.868、4.695화3.406,P균〈0.05）;이상각세포단백적면역세포화면역인적신호지간정정상관（rs분별위0.952、0.915、0.927、0.842、0.879화0.855,P균〈0.05）。결론：nLQ가억제Eca-9706세포생장급증식,역전Eca-9706세포PTEN적저표체화c-Met급VEGF적고표체,병통과억제HDAC1화NF-κB급격활PTEN표체적HDAC억제신호도경이유도세포조망。
Aim：To explore the mechanism for reverse transformation and apoptosis of Eca-9706 cells induced by nanoliposomal quercetin（nLQ）.Methods：A kind of liposomal quercetin, with chloroform＋DMSO being used as solvents,was prepared through rotary evaporation, and the nLQ was obtained after ultrasonic disruption and filtration.The cultured Eca-9706 cells were treated with nLQ at different concentrations,and cell growth inhibition rate for different exposure time （24,48,and 72 h） was detected by MTT.Eca-9706 cells were allocated into nLQ group （given 40 μmol/L nLQ） and control group.Apoptotic rate in the 2 groups was detected by TUNEL.After 48-hour-exposure,the expression of Cyclin D1,PTEN,c-Met,VEGF,HDAC1 and NF-κB in the 2 groups were detected by immunohistochemistry and immunoblotting.Results：Compared with the control group, the growth-inhibition rate （F24 h=128.041,F48 h=142.683 and F72 h=231.054,P0.001）and apoptotic rate（F=94.770,P0.001） of the groups of Eca-9706 cells had difference. The immunohistochemistry and immunoblotting showed that the expression of PTEN was up-regulated（t=5.352 and 4.308,P0.05）, while the immunohischemistry results of Cyclin D1, c-Met, VEGF,HDAC1 and NF-κB were down-regulated（t=4.006,9.184,13.853,4.698 and 3.575,P0.05）, and their immunoblotting results were also down-regulated（t=3.827,6.399,7.868,4.695 and 3.406,P0.05）.There was positive correlation in data above between immunocytochemistry and immunoblotting（rs=0.952,0.915,0.927,0.842,0.879,and 0.855,P0.05）.Conclusion：The Eca-9706 cell growth and proliferation could be inhibited by nLQ, and the overexpression of c-Met and VEGF and the low expression of PTEN in Eca-9706 cells could be reversed by nLQ. The Eca-9706 cells apoptosis could be induced through inhibiting HDAC1 and NF-κB and activating PTEN expressions.