M-CSF

摘要： 目的探讨巨噬细胞集落刺激因子(M-CSF)、糖类抗原153(CA153)、人乳头瘤病毒(HPV)联合检测在宫颈癌早期筛查中的临床意义。方法选择2017年5月至2019年8月于本院诊治的192例疑似宫颈癌患者为研究对象,检测患者的M-CSF、CA153、HPV等指标,并以病理检查结果为最终诊断,计算M-CSF、CA153、HPV单独检测及联合检测的灵敏度、特异度、诊断符合率、假阳性率、假阴性率等,并比较不同类型患者的M-CSF、CA153表达水平和HPV病毒载量,采用Logistic多元回归分析以上指标与宫颈癌的相关性。结果M-CSF、CA153、HPV单独检测的诊断符合率依次为68.23%、66.15%、65.10%,与联合检测的92.19%相比较低(P<0.05);与联合检测相比,各单项检测的灵敏度、特异度、诊断符合率较低,假阴性率、假阴性率较高(P<0.05);阳性患者CINⅠ、CINⅡ、CINⅢ及宫颈癌患者M-CSF、CA153水平及HPV病毒载量均高于阴性患者,且随着病情加重呈递增趋势(P<0.05)。经Logistic多元回归分析发现,宫颈癌与血清M-CSF、CA153水平及HPV病毒载量均为正相关,OR值依次为1.022、1.704、1.289。结论M-CSF、CA153、HPV均为宫颈癌诊断的重要指标,其表达水平可随患者病情发展而变化,均属于宫颈癌独立危险因素,联合检测M-CSF、CA153、HPV在宫颈癌早期筛查中有重要价值。

摘要： 目的 探讨并分析急性脑梗死(ACI)患者血清氧化低密度脂蛋白(ox-LDL)、巨噬细胞集落刺激因子(M-CSF)、脂蛋白相关磷脂酶(Lp-PLA2)水平变化对其神经功能的影响.方法 选取2018年9月至2020年9月莆田市第一医院接诊的148例ACI患者为研究对象,根据美国国立卫生研究院卒中量表(NIHSS)评分将患者分为轻度组(43例)、中度组(59例)和重度组(46例).回顾性分析不同程度神经功能损伤患者血清ox-LDL、M-CSF及Lp-PLA2水平变化,并采用Spearman检验对患者神经功能损伤程度与血清ox-LDL、M-CSF及Lp-PLA2水平进行相关性分析.结果 ACI患者随着其神经功能损伤程度的递增,血清ox-LDL、M-CSF及Lp-PLA2水平均递增,两者成正相关.结论 ACI患者血清ox-LDL、M-CSF、Lp-PLA2水平变化与患者神经功能损伤密切相关,且水平越高,患者神经功能损伤越严重,临床可通过监测患者血清ox-LDL、M-CSF、Lp-PLA2水平预测患者神经功能的恢复情况.

摘要： 目的:观察加服健心平律丸对冠心病心绞痛患者血清炎症因子的影响.方法:将80例冠心病心绞痛气虚痰瘀证患者随机分为2组,对照组40例予抗血小板聚集、扩张血管(β受体阻滞剂、硝酸酯类药物)等西医基础治疗;治疗组40例在对照组治疗基础上口服健心平律丸(组成:太子参、黄芪、丹参、半夏、竹茹、橘红、枳壳、酸枣仁、麦冬等)每次6 g,每天3次.两组治疗以90天为1个疗程,1个疗程后观察比较两组治疗前后血清巨噬细胞集落刺激因子(M-CSF)、内皮素(ET)、白细胞介素-18(IL-18)水平.结果:两组治疗后血清ET、IL-18、M-CSF水平较治疗前显著降低(P0.05).结论:加服健心平律丸能降低冠心病心绞痛患者M-CSF、ET、IL-18水平,降低血清ET水平优于单用西药组,且无不良反应.

摘要： To explore the effect and mechanisms of cytoplasmic M-CSF on glucose metabolism in human breast cancer MCF-7 cells,MCF-7 cells stable expressing cytoplasmic M-CSF were constructed.Relative ATP content was measured by ATP assay kit,glucose was measured using glucose assay kit and lactate was measured using lactate acid assay kit.The expression of HK2,PKM2 and GLUT-1 in three kinds of cell with LY294002 or API-2 was detected by West-blotting.The sensitivity of MCF-7 and MCF-7-M cells to 5-FU with the treatment of ATP depletion by 3-BrPA was observed by MTT assay.It was found that the ATP level of MCF-7-M cells was significantly higher than that of MCF-7 cells(P<0.05);2-DG decreases the ATP level of MCF-7 and MCF-7-M cells,and the effect of lowering the ATP level of MCF-7-M cells is more obvious(P<0.01).The glucose uptake and lactate secretion of MCF-7-M cells were significantly higher than those of MCF-7 cells(P<0.01).After the treatment with API-2,the glucose consumption and lactate secretion of MCF-7 and MCF-7-M cells were significantly reduced(P<0.01).The expressions of GLUT-1,HK2 and PKM2 in MCF-7-M cells were significantly higher than those in MCF-7 cells(P<0.01).Both LY294002 and API-2 inhibited the expression of GLUT-1 in MCF-7-M cells(P<0.05).After the treatment with 3-BrPA,the drug sensitivity of MCF-7-M and MCF-7 cells to 5-FU was significantly enhanced(P<0.01).In conclusion,cytoplasmic M-CSF activates glycolysis by induce GLUT-1,HK2 and PKM2 protein expression in MCF-7 cells;PI3K/AKT signaling involves the pathway that glycolysis was activated by cytoplasmic M-CSF in MCF-7 cells.%本文探讨巨噬细胞集落刺激因子(M-CSF)对人乳腺癌MCF-7细胞糖代谢的影响及其机制.构建胞质稳定转染M-CSF的MCF-7细胞(MCF-7-M);ATP检测试剂盒检测MCF-7和MCF-7-M细胞的ATP生成;葡萄糖测定试剂盒、乳酸测试盒检测MCF-7和MCF-7-M细胞的葡萄糖摄取和乳酸分泌情况;蛋白质印迹法检测在糖酵解抑制剂2-脱氧葡萄糖(2-DG)和氧化磷酸化抑制剂OLIG处理后,M-CSF对MCF-7细胞的糖酵解关键酶:己糖激酶2(HK2)、丙酮酸激酶M2(PKM2)及葡萄糖转运体1(GLUT-1)表达的影响;MTT法检测在ATP消耗剂3-溴丙酮酸(3-BrPA)处理后,MCF-7和MCF-7-M细胞对5-FU敏感性的变化.结果发现:MCF-7-M细胞的ATP水平显著高于MCF-7细胞(P<0.05);2-DG降低了MCF-7和MCF-7-M细胞的ATP水平,并且降低MCF-7-M细胞ATP的效果更明显(P<0.01);MCF-7-M细胞的糖摄取能力和乳酸分泌量显著高于MCF-7细胞(P<0.01),经API-2处理后,MCF-7和MCF-7-M细胞葡萄糖消耗和乳酸分泌量均显著减少(P<0.01);MCF-7-M细胞GLUT-1、HK2和PKM2的表达显著高于MCF-7细胞(P<0.01);LY294002和API-2均可抑制MCF-7-M细胞GLUT-1的表达(P<0.05);用3-BrPA处理后,MCF-7-M和MCF-7细胞对5-FU的药物敏感性显著增强(P<0.01).综上,得出结论:胞质M-CSF通过诱导GLUT-1、HK2和PKM2的表达,活化MCF-7细胞糖酵解途径;PI3K/AKT信号通路参与胞质M-CSF活化MCF-7细胞的糖酵解途径.

摘要： 目的:研究雌二醇对MCF-7细胞教化单核细胞分化为肿瘤相关巨噬细胞的影响.方法:分别用10 nM雌二醇及10 nM雌二醇+1μM他莫昔芬处理雌激素受体阳性乳腺癌细胞株MCF-7, 48 h后收集细胞培养上清, 利用细胞因子芯片检测不同处理组单核细胞活化相关蛋白与空白对照组MCP-1及M-CSF的表达差异, 利用细胞Transwell niche检测其对单核细胞活化功能的影响.结果:Bio-Rad细胞因子芯片检测发现空白对照组、雌二醇组及雌二醇+他莫昔芬组细胞上清中CSF1浓度分别为 (1.83±0.18), (29.71±8.06) 及 (10.90±2.38) pg/m L, MCP-1分别为 (31.33±2.40), (75.37±5.50) 和 (41.97±5.80) pg/m L, 比较差异均有统计学意义 (P<0.05) .雌二醇处理组CD163的mRNA水平是对照组 (76.83±12.80) 倍, 他莫昔芬加雌二醇组是对照组的 (6.5±1.71) 倍, 比较差异有统计学意义 (F=96, P<0.01) .对照组、雌二醇处理组及他莫昔芬加雌二醇处理组每个高倍镜视野内U937细胞数目分别为 (28±6) 、 (188±16) 及 (82±9) 个, 比较差异有统计学意义 (F=160, P<0.05) .结论:雌二醇通过上调激素依赖型乳腺癌细胞株MCF-7表达M-CSF从而增强其对单核细胞的教化, 而他莫昔芬可部分阻断其发挥效应.%Objective:To investigate the effect of Estradiol on educating monocyte differentiation into tumor associated macrophage in MCF-7 coculture system.Method:48 h after treated with 10 nM Estradiol or10 nM Estradiol+1μM Tamoxifen, MCP-1 and M-CSF in human breast cancer cell line MCF-7 culture supernatant were detected, they were given Transwell niche to further explore their effects on the recruitment and activation of monocyte.Result:Bio-Rad cytokine chip assay showed that the M-CSF concentration in the supernatant of blank control group, Estradiol group and Estradiol+Tamoxifen group were (1.83±0.18), (29.71±8.06) and (10.90±2.38) pg/mL, and the MCP-1 concentration were (31.33±2.40), (75.37±5.50) and (41.97±5.80) pg/mL respectively, the differences were statistically significant (P<0.05).The level of CD163 mRNA in estradiol treatment group was (76.83±12.80) times higher than that in control group, and that in Estradiol+Tamoxifen group was (6.50±1.71) times higher than that in control group (F=96, P<0.01).The number of U937 cells in the control group, the Estradiol treatment group and the Estradiol+Tamoxifen treatment group were (28±6), (188±16) and (82±9) respectively, the difference was statistically significant (F=160, P<0.05).Conclusion:Estradiol may promote hormone dependent breast cancer cell lines MCF-7 to secrete MCP-1 and M-CSF, thereby educate monocyte differentiation into tumor associated macrophage, while Tamoxifen may partially block the effect.

摘要： 目的:分析阿尔茨海默病血浆中 β 淀粉样蛋白1-40(Aβ1-40)、血脂指标及相关炎症因子的临床意义.方法:择取收治的85例阿尔茨海默病患者作为研究对象,按照阿尔茨海默病评定量表-认知量表(ADAS-Cog)分为两组,轻度组(ADAS-Cog总分0.05).AD两组血浆中Aβ1-40、IL-6、M-CSF、IL-1β、TNF-α 水平均高于对照组,除M-CSF外,差异均有统计学意义;中重度组除M-CSF明显低于轻度组外,IL-6、IL-1β、TNF-α 均明显高于轻度组,差异均有统计学意义(P0.05).结论:阿尔茨海默病患者的Aβ1-40、血脂水平及相关炎症因子水平均有所升高,其中相关炎症因子与疾病的发生发展呈正相关,这些指标或对临床诊断有一定意义.

摘要： The etiology and pathogenesis of pulmonary fibrosis is poorly understood. We and others reported that M-CSF/CSF-1, M-CSF-R and downstream AKT activation plays an important role in lung fibrosis in mice models and in IPF patients. To understand potential molecular pathways used by M-CSF-R activation to direct lung fibrosis, we used a novel transgenic mouse model that expresses a constitutively-active form of AKT, myristoylated AKT (Myr-Akt), driven by the c-fms (M-CSF-R) promoter. We were particularly interested in the basal immune state of the lungs of these Myr-Akt mice to assess M-CSF-R-related priming for lung fibrosis. In support of a priming effect, macrophages isolated from the lungs of unchallenged Myr-Akt mice displayed an M2-tropism, enhanced co-expression of M-CSF-R and α-SMA, reduced autophagy reflected by reduced expression of the key autophagy genes Beclin-1, MAP1-Lc3a(Lc3a), and MAP1-Lc3b(Lc3b), and increased p62/STSQM1 expression compared with littermate WT mice. Furthermore, Myr-Akt mice had more basal circulating fibrocytes than WT mice. Lastly, upon bleomycin challenge, Myr-Akt mice showed enhanced collagen deposition, increased F4/80+ and CD45+ cells, reduced autophagy genes Beclin-1, Lc3a, and Lc3b expression, and a shorter life-span than WT littermates. These data provide support that M-CSF-R/AKT activation may have a priming effect which can predispose lung tissue to pulmonary fibrosis.