發(fā)布時間：2018-05-27 15:19

  本文選題：肺癌細(xì)胞株A549 + M1型巨噬細(xì)胞��； 參考：《河北醫(yī)科大學(xué)》2017年碩士論文

【摘要】：目的:順鉑是治療非小細(xì)胞肺癌的有效藥物之一,但臨床上發(fā)現(xiàn)隨著治療周期次數(shù)的增加,癌細(xì)胞對順鉑的敏感性逐漸降低,最后出現(xiàn)對順鉑耐受。目前普遍認(rèn)為腫瘤相關(guān)巨噬細(xì)胞(tumor associated macrophage,TAM)作為腫瘤微環(huán)境的重要基質(zhì)細(xì)胞,不僅直接參與腫瘤血管的形成,而且通過與腫瘤細(xì)胞間的相互作用,介導(dǎo)腫瘤細(xì)胞的間質(zhì)轉(zhuǎn)化,促進(jìn)腫瘤轉(zhuǎn)移。根據(jù)巨噬細(xì)胞的表型和功能,巨噬細(xì)胞分為M1型和M2型;且近期的研究表明M1和M2型巨噬細(xì)胞在腫瘤組織中均有分布。但是M1和M2型巨噬細(xì)胞對肺癌細(xì)胞的增殖、遷移及對順鉑敏感性的作用如何還鮮有報道。本實驗采用A549細(xì)胞及其荷瘤小鼠為模型,觀察了M1和M2型巨噬細(xì)胞及其分泌的外泌體在體內(nèi)外對A549細(xì)胞的增殖、遷移及對順鉑敏感性的作用,目的是深入了解不同類型的巨噬細(xì)胞對順鉑治療的影響,為靶向調(diào)節(jié)巨噬細(xì)胞促進(jìn)順鉑治療效果提供實驗數(shù)據(jù)。方法:1 M1和M2巨噬細(xì)胞的誘導(dǎo)體外培養(yǎng)人單核細(xì)胞白血病細(xì)胞系THP-1,PMA(15μg/ml)誘導(dǎo)36h,去掉含PMA的培養(yǎng)基并用PBS洗一遍,加入新鮮完全培養(yǎng)基繼續(xù)培養(yǎng)12h,貼壁的細(xì)胞為M0。1.1 M1細(xì)胞的誘導(dǎo):貼壁細(xì)胞用含1μg/ml脂多糖(LPS)和20ng/ml人重組干擾素-γ(IFN-γ)的完全培養(yǎng)基培養(yǎng)24h,然后去掉培養(yǎng)上清,PBS洗1次,加入新鮮完全培養(yǎng)基培養(yǎng)24h,收獲上清經(jīng)ELISA測定IL-1β水平,收集細(xì)胞提取總蛋白,Western blot分析i NOs(誘導(dǎo)型一氧化碳合酶)、Arg-1(精氨酸酶-1)的表達(dá)。1.2 M2細(xì)胞的誘導(dǎo):貼壁細(xì)胞用含20ng/ml IL-4的完全培養(yǎng)基培養(yǎng)24h,然后去掉培養(yǎng)上清,PBS洗1次,去掉殘存的細(xì)胞因子或LPS,加入新鮮完全培養(yǎng)基培養(yǎng)24h,收獲上清(ELISA測定IL-1β),收細(xì)胞,WB分析i NOs、Arg-1的表達(dá)。2外泌體的制備及電鏡觀察收集M1型和M2型巨噬細(xì)胞培養(yǎng)上清,差速離心法分離提取外泌體(M1/exo,M2/exo):2000×g,10min,10,000×g,1h;然后將上清超高速110,000×g離心16 h,以少量PBS重懸所得沉淀。最后用磷鎢酸負(fù)染外泌體并在透射電鏡下觀察外泌體的形態(tài),并以Nanodrop進(jìn)行定量。3觀察M1/exo,M2/exo對A549細(xì)胞增殖、遷移及對順鉑敏感性的影響3.1 Dil熒光染料標(biāo)記M2/exo:取11.5mg/ml的M2/exo0.5ml,加Dil熒光染料(50μg/ml),25μg,放培養(yǎng)箱中作用30分鐘,取出放入小的超速離心管中,用PBS補滿,上超速離心機,2×105g轉(zhuǎn)速,2小時,離心后棄上清,去掉游離的染料,要沉淀外泌體。將熒光標(biāo)記的外泌體作用于A549細(xì)胞24h,熒光顯微鏡下觀察A549對外泌體的攝取。3.2體外培養(yǎng)A549細(xì)胞,分別用終濃度50μg/ml的M1/exo或M2/exo刺激A549細(xì)胞,Transwell細(xì)胞遷移實驗、劃痕試驗分別觀察兩種不同外泌體對A549遷移能力的影響。3.3用艾森生物實時細(xì)胞分析技術(shù)(RTCA),即實時無標(biāo)記細(xì)胞分析法,檢測M1/exo或M2/exo刺激對A549增殖和對順鉑耐藥性的影響。4觀察M1/exo或M2/exo對A549細(xì)胞的E-Cadherin、N-Cadherin、PTEN、AKT/p-AKT蛋白表達(dá)的影響體外培養(yǎng)A549細(xì)胞,M1/exo或M2/exo刺激72h,收集細(xì)胞并提取總蛋白,Western Blot分析上述蛋白表達(dá)。5 M1及M2型巨噬細(xì)胞及其分泌的外泌體影響A549荷瘤小鼠腫瘤生長及對順鉑敏感性的觀察5.1細(xì)胞培養(yǎng)與計數(shù)收集體外培養(yǎng)的處于對數(shù)生長期A549計數(shù),調(diào)整細(xì)胞密度為7×107/ml。同1.1和1.2誘導(dǎo)M1型和M2型巨噬細(xì)胞,計數(shù)后,分別調(diào)整細(xì)胞密度為7×107/ml。5.2荷瘤小鼠的制備5.2.1實驗分組將5-6周的雌性BALB/c裸鼠分為10組,每組5只。第一組:A549荷瘤對照組。將體外培養(yǎng)的A549移植到小鼠右側(cè)腋下,7×106/鼠。第二組:A549+M1組。取等量的A549和M1型細(xì)胞(均100μl)混合后,移植到小鼠右側(cè)腋下。第三組:A549+M2組。取等量的A549和M2型細(xì)胞(均100μl)混合后,移植到小鼠右側(cè)腋下。第四組:A549+順鉑。右側(cè)腋下移植A549,7×106/鼠,按Q4d×3的方案腹腔注射順鉑(5mg/kg)。第五組:A549+M1+順鉑。同上移植A549和M1,腹腔注射順鉑。第六組:A549+M2+順鉑。同上移植A549和M2,腹腔注射順鉑。第七組:A549+M1/exo。同上移植A549,在移植的當(dāng)天,在注射腫瘤細(xì)胞的部位注射50μg外泌體。隔日一次,連續(xù)3周。第八組:A549+M2/exo。同上移植A549和外泌體注射。第九組:A549+M1/exo+順鉑。同上。第十組:A549+M2/exo+順鉑。同上。5.3觀察腫瘤瘤重在荷瘤的第四周,解剖荷瘤小鼠,分離腫瘤組織并稱重。結(jié)果:1 ELASA法檢測誘導(dǎo)的M1型巨噬細(xì)胞上清液中IL-1β含量低于M2型巨噬細(xì)胞組,差異具有統(tǒng)計學(xué)意義(P0.05)。M1型巨噬細(xì)胞i NOs(誘導(dǎo)型一氧化碳合酶)蛋白表達(dá)量明顯高于M2型巨噬細(xì)胞(P0.05);Arg-1(精氨酸酶-1)蛋白表達(dá)量低于M2型巨噬細(xì)胞(P0.05)。體外成功誘導(dǎo)M1型巨噬細(xì)胞、M2型巨噬細(xì)胞。2電鏡觀察到大小均一的、直徑約為100 nm大小的圓形或橢圓形囊泡。3倒置熒光顯微鏡下觀察到A549細(xì)胞可以攝取外泌體。4劃痕實驗觀察到,PBS、M1/exo對A549的橫向遷移沒有明顯影響(P0.05);M2/exo可促進(jìn)A549細(xì)胞的橫向遷移(P0.05)。Transwell實驗顯示,M2/exo較對照組及M1/exo組明顯促進(jìn)A549細(xì)胞的縱向遷移(P0.05),M1/exo的作用不明顯(P0.05)。細(xì)胞增殖實驗顯示M2/exo可促進(jìn)A549細(xì)胞的增殖和降低對順鉑的敏感性。5 Western blot結(jié)果顯示,與PBS及M1/exo相比較,M2/exo明顯上調(diào)A549細(xì)胞N-Cadherin的表達(dá)(P0.05),下調(diào)E-Cadherin表達(dá)水平(P0.05);表明M2/exo能夠促進(jìn)A549發(fā)生間質(zhì)轉(zhuǎn)化和遷移。A549細(xì)胞經(jīng)M1/exo和M2/exo刺激后,PTEN表達(dá)水平在M2/exo刺激組明顯低于M1/exo刺激組和對照組(P0.05)。p-AKT(p-AKT/AKT灰度值)活力水平在M2/exo刺激組增高,且顯著高于M1/exo刺激組和對照組(P0.05)。6小鼠荷瘤實驗結(jié)果顯示1)A549+M2細(xì)胞組荷瘤小鼠的瘤重明顯大于A549組和A549+M1細(xì)胞組,均有顯著差異(均為P0.01)。A549+M1細(xì)胞組和A549組瘤重比較無顯著差異(P0.05)。以上結(jié)果顯示M2細(xì)胞可以促進(jìn)A549瘤體增殖。2)A549細(xì)胞、A549+M2細(xì)胞及A549+M1細(xì)胞三組荷瘤小鼠分別經(jīng)順鉑治療后,觀察到A549+M2細(xì)胞組瘤重最大,與其它兩組均有顯著性差異(均為P0.05)。而M1+A549與A549細(xì)胞組的瘤重?zé)o統(tǒng)計學(xué)差異(P0.05)。3)給A549荷瘤小鼠瘤周注射M2/exo組瘤重最大,與注射M1/exo和PBS組的瘤重相比,均有統(tǒng)計學(xué)差異(均為P0.05);A549荷瘤小鼠瘤周注射M1/exo和PBS組的瘤重沒有顯著差別(P0.05)。4)A549荷瘤小鼠瘤周注射M2/exo后,對順鉑的治療敏感性較差,該組荷瘤小鼠瘤重與注射M1/exo和PBS組的瘤重相比,均有統(tǒng)計學(xué)差異(均為P0.05);而M1/exo和PBS均不影響A549細(xì)胞對順鉑的敏感性。結(jié)論:1 M2型巨噬細(xì)胞可促進(jìn)A549細(xì)胞增殖、遷移,并降低對順鉑敏感性。2 M2型巨噬細(xì)胞產(chǎn)生的外泌體可促進(jìn)A549細(xì)胞增殖、遷移,并降低對順鉑敏感性。
[Abstract]:Objective: cisplatin is one of the effective drugs for the treatment of non-small cell lung cancer. However, it is found that the sensitivity of cancer cells to cisplatin gradually decreases with the increase of the number of treatment cycles, and the tumor associated macrophage (TAM) is widely considered as an important matrix of tumor microenvironment. Cells not only directly participate in the formation of tumor vessels, but also mediate interstitial transformation of tumor cells and promote tumor metastasis through interaction with tumor cells. According to the phenotype and function of macrophages, macrophages are divided into M1 type and M2 type. And recent studies have shown that M1 and M2 type macrophages are distributed in tumor tissues. But M1 The effects of M2 type macrophages on proliferation, migration and sensitivity to cisplatin are rarely reported. This experiment uses A549 cells and tumor bearing mice as models to observe the proliferation, migration and sensitivity to cisplatin by M1 and M2 macrophages and the secreted exocrine in vivo and in vivo. To understand the effect of different types of macrophages on cisplatin treatment and to provide experimental data for the targeting of macrophages to promote cisplatin treatment. Methods: 1 M1 and M2 macrophages were induced in vitro to induce human monocytic leukemia cell line THP-1, PMA (15 g/ml) to induce 36h, remove PMA containing medium and wash it with PBS to add fresh finish. The whole culture medium continued to culture 12h, the adherent cells were induced by M0.1.1 M1 cells: adherent cells cultured 24h with 1 mu g/ml lipopolysaccharide (LPS) and 20ng/ml human recombinant interferon gamma (IFN- gamma) complete medium, then removed culture supernatant, PBS washed 1 times, added fresh complete medium to culture 24h, and harvested supernatant to determine IL-1 beta level by ELISA. Cell extraction of total protein, Western blot analysis of I NOs (inducible carbon monoxide synthase), Arg-1 (arginase -1) expression of.1.2 M2 cells induced: adherent cells cultured with 20ng/ml IL-4 containing full medium culture 24h, and then removed the culture supernatant, PBS washed 1 times, remove the remaining cytokine or paste, add fresh complete medium culture, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest, harvest (ELISA determination of IL-1 beta), cell collection, WB analysis of I NOs, Arg-1 expression of.2 exocrine and electron microscope observation to collect M1 and M2 type macrophage culture supernatant, differential centrifugation separation and extraction of exocrine (M1/exo, M2/exo): 2000 * g, 10000 * centrifugation, and then superhigh speed 110000 x centrifugation 16 The morphology of exocrine was observed by negative staining with phosphotungstic acid and under transmission electron microscope. The effects of M1/exo, M2/exo on A549 cell proliferation, migration and cisplatin sensitivity were observed by Nanodrop, and the effect of M2/exo on the M2/exo0.5ml of 11.5mg/ml by 3.1 Dil fluorescent dye M2/exo:, Dil fluorescein (50 mu g/ml), 25 micron g, and 30 minutes in the incubator. The clock was taken out into a small overspeed centrifuge tube, filled with PBS, overspeed centrifuge, 2 x 105g speed, 2 hours, after centrifugation, discarding the supernatant, removing the free dye, and precipitating the exocrine. The fluorescence labeled exocrine was acted on the A549 cell 24h, and the fluorescence microscope observed the uptake of A549 to the exocrine by.3.2 in the culture of A549 cells in vitro. The final concentration was used respectively. 50 g/ml M1/exo or M2/exo stimulates A549 cells, Transwell cell migration experiments, and scratch test to observe the effect of two different exocrine on the migration ability of A549,.3.3 using Eisen biological real-time cell analysis technique (RTCA), that is, real time unlabeled cell analysis, to detect the effect of M1/exo or M2/exo stimulation on A549 proliferation and cisplatin resistance. 4 the effects of M1/exo or M2/exo on the expression of E-Cadherin, N-Cadherin, PTEN, and AKT/p-AKT protein in A549 cells were affected in the culture of A549 cells in vitro. M1/exo or M2/exo stimulated 72h, collecting cells and extracting the total protein. Cisplatin sensitivity observation 5.1 cell culture and count collection in the logarithmic growth period A549 count, adjust cell density to 7 x 107/ml. with 1.1 and 1.2 induction of M1 and M2 type macrophages, after counting, the cell density of 7 * 107/ml.5.2 bearing mice in the preparation of 5.2.1 experiment group for 5-6 weeks female BALB/c nude mice 10 groups, each group of 5. A549 tumor bearing control group. Transplanted A549 in vitro to the right underarm of mice, 7 x 106/ mice. Group second, group A549+M1. The same amount of A549 and M1 cells (100 mu L) were mixed and transplanted into the right arm of the mouse. The third group: A549+M2 group. After mixing the same amount of A549 and M2 cells (100 um L), transplanted into mice. Right axillary subaxillary. Fourth groups: A549+ cisplatin. Right subaxillary transplantation of A549,7 x 106/ mice, intraperitoneal injection of cisplatin (5mg/kg) by Q4d x 3. Group Fifth: A549+M1+ cisplatin. Co transplantation of A549 and M1, intraperitoneal injection of cisplatin. Group sixth: A549+M2+ cisplatin. Co transplantation of A549 and M2, abdominal injection cisplatin. Seventh groups: A549+M1/exo. same transplant recipients, transplanted in transplant On the same day, 50 g exosecrete was injected at the site of the injection of tumor cells. One time every other day for 3 weeks. Group eighth: A549+M2/exo. combined with A549 and exosecrete. Ninth group: A549+M1/exo+ cisplatin. Tenth groups: A549+M2/exo+ cisplatin. Same.5.3 observed tumor weight in the fourth week of the tumor, dissecting tumor bearing mice, separating tumor tissue and weighing Results: results: the content of IL-1 beta in the induction of M1 macrophage supernatant by 1 ELASA method was lower than that of M2 macrophage group, and the difference was statistically significant (P0.05).M1 macrophage I NOs (inducible carbon monoxide synthase) protein expression was significantly higher than that of M2 type macrophage (P0.05), Arg-1 (arginase -1) protein expression was lower than that of macrophage Cell (P0.05). M1 macrophages were successfully induced in vitro. The.2 electron microscopy of M2 type macrophages showed that the size of the size was uniform, and the diameter of the round or oval vesicle with a diameter of 100 nm was observed under the.3 inverted fluorescence microscope, and the A549 cells could be observed in the Exocyst.4 scratch test. PBS, M1/exo had no significant influence on A549 lateral migration (P0.05). Exo could promote the lateral migration of A549 cells (P0.05).Transwell experiment, which showed that M2/exo significantly promoted vertical migration of A549 cells (P0.05) compared with the control group and M1/exo group, and the effect of M1/exo was not obvious (P0.05). Compared with M1/exo, M2/exo obviously up-regulated the expression of N-Cadherin in A549 cells (P0.05), and down regulated the E-Cadherin expression level (P0.05), indicating that M2/exo can promote the transformation of A549 and the migration of.A549 cells after M1/exo and M2/exo stimulation. The activity level was higher in the M2/exo stimulation group and was significantly higher than that in the M1/exo stimulation group and the control group (P0.05).6 mice. The tumor bearing tumor weight of the A549+M2 cell group was significantly greater than that of the A549 group and the A549+M1 cell group. There was significant difference (P0.05 P0.01) between the.A549+M1 cell group and the A549 group (P0.05). The above results showed that M2 cells could promote the proliferation of A549 tumor.2) A549 cells, and the three groups of A549+M2 and A549+M1 cells were treated with cisplatin, respectively. The tumor weight of the A549+M2 cell group was the largest, and the difference between the other two groups was significant (P0.05). There was no statistical difference between the M1+A549 and A549 cell groups (P0.05).3) The tumor weight in the M2/exo group was the largest in the tumor bearing mice. Compared with the injection of M1/exo and PBS, there were statistically significant differences (all P0.05). The tumor weight of A549 mice injected with M1/exo and PBS was not significantly different (P0.05).4) in A549 bearing mice (P0.05).4), the sensitivity to cisplatin was poor in the treatment of cisplatin, and the tumor weight of this group of tumor bearing mice was heavy. Compared with the tumor weight of the M1/exo and PBS groups, there were statistically significant differences (both P0.05), while both M1/exo and PBS did not affect the sensitivity of A549 cells to cisplatin. Conclusion: 1 M2 macrophages can promote the proliferation, migration and decrease of the exoss produced by the cisplatin sensitive.2 M2 type macrophages, which can promote the proliferation, migration, and decrease of A549 cells. Low sensitivity to cisplatin.
【學(xué)位授予單位】：河北醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R73-36

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