苹果提取物抑制肝癌细胞系生长的实验性研究

目的观察苹果提取物在体外对肝癌细胞系(HepG2)生长的抑制作用.方法新鲜富士苹果利用丙酮法提取,不同浓度苹果提取物与Hepg2细胞系混合培养,利用MTS法检测提取物对于肿瘤细胞生长的抑制程度.结果富士苹果提取物对于HepG2细胞生长有一定程度的抑制作用,在50mg/ml时,抑制率达39.03%.结论苹果提取物在体外具有抑制肝癌细胞系生长的作用.     

获得性顺铂耐药的大肠腺癌LS-174T细胞核中YB-1的活性改变及其对P-gp和PCNA转录表达的影响

目的:观察耐药细胞株LS-174T核中YB-1的活性改变及其对P-gp和PCNA转录表达水平的影响,探讨YB-1在肿瘤顺铂耐药机制中的作用。方法:采用顺铂药物浓度递增法、间歇性作用的体外诱导法建立人结肠癌的多重耐药细胞系LS-174T;用EMSA检测耐药肿瘤细胞核中转录因子YB-1活性的改变,半定量RT-PCR检测P-gp和PCNA mRNA表达水平的改变。结果:耐药细胞株核中YB-1的活性明显增加,且P-gp mRNA和PCNA mRNA的表达水平均较非耐药细胞株明显增高(P<0.01)。结论:顺铂耐药细胞株细胞核内YB-1活性增高促进了P-gp和PCNA转录表达水平,它们可能共同参与顺铂导致DNA损伤的修复,在肿瘤耐药机制中发挥重要作用。     

去甲斑蝥素通过JAK-STAT3途径诱导结肠癌LS-174T细胞凋亡

目的 探讨去甲斑蝥素(NCTD)诱导结肠癌LS-174T细胞的凋亡效应及其可能分子机制。方法 应用MTT法检测NCTD对细胞生长的抑制作用,通过AO/EB染色、透射电子显微镜观察细胞形态及超微结构的变化,AnnexinV/PI染色检测细胞凋亡率,Western blot检测stat3、survivin、Mcl-1、bax蛋白的表达情况。结果 去甲斑蝥素对结肠癌LS-174T细胞具有显著的生长抑制作用,并呈时间—剂量依赖性;40 μg/ml作用72 h时达到最大抑制率(72.4±3.1)%;AO/EB染色及流式细胞术显示,随着NCTD浓度的增加,细胞凋亡率明显增加;透射电子显微镜观察发现,结肠癌LS-174T细胞出现明显凋亡超微结构变化;Western blot结果显示,stat3、survivin、Mcl-1表达明显下降,bax表达明显上升。结论 去甲斑蝥素可以抑制结肠癌LS-174T细胞的生长并促进其凋亡,机制可能是通过抑制stat3途径实现的。     

三氧化二砷的抗大肠癌作用及其机制

目的观察三氧化二砷(As2O3)对大肠癌LS-174T细胞生长及端粒酶活性的影响。方法As2O3作用于大肠癌LS-174T细胞和裸鼠移植瘤后,采用噻唑盐(MTT)比色法检测结肠癌细胞生长抑制情况,电镜检测细胞超微结构的改变,荧光染色观察细胞核形态变化,流式细胞术(FCM)检测As2O3对细胞周期的影响,聚合酶链反应-酶联免疫反应(PCR-ELISA)试剂盒检测细胞中端粒酶活性变化。结果MTT法显示,随着As2O3浓度的升高,LS-174T细胞存活率明显下降,IC50= 5.23μmol/L。As2O3作用于LS-174T细胞24 h即出现凋亡峰,凋亡细胞的数量随着作用时间增加而增加。As2O3对LS-174T细胞提取液端粒酶活性有一定的抑制作用,对癌细胞端粒酶活性抑制作用随作用时间的延长而加强。从实验动物瘤体积和瘤重两个指标分析,As2O3组与对照组相比具有明显的抑癌作用(P<0.05)。结论经体外、体内实验证实,As2O3对结肠癌LS-174T细胞生长和裸鼠移植瘤均有抑制作用,其抗癌机制可能与诱导细胞凋亡和抑制端粒酶活性有关。     

金属硫蛋白对人宫颈癌细胞增殖和凋亡的影响

 目的 探讨金属硫蛋白（metallothionein，MT）对人宫颈癌细胞HeLa增殖和凋亡的影响并初步分析其机制。方法 以不同浓度的MT（0．001、0．01、0．1和1ng／m1）干预HeLa细胞，MTT法测定其对细胞 增殖的促进作用，流式细胞仪分析凋亡率，免疫细胞化学法和RT-PIER法测定p53和PCNA的表达。结果 （1）MT对HeLa细胞增殖表现出浓度依赖性的促进作用，以1ng／ml时作用最明显（P〈0．05）。（2）MT可抑制细胞凋亡，其浓度为0、0．01和1ng／ml时，凋亡指数（AJ）分别为（6．35±1．08）％、（4．45±0．95）％和（2．15±0．77）％。（3）MT作用后细胞p53表达显著减弱，PCNA表达显著增强，两者均呈浓度依赖性。结论 MT对人宫颈癌HeLa细胞具有显著地促进增殖和抑制凋亡作用，其机制可能与抑制p53基因表达有关。     

Aqueous extract of Curcuma aromatica induces apoptosis and G2/M arrest in human colon carcinoma LS-174-T cells independent of p53

Curcuma aromatica is a common Chinese herb for treating diseases with blood stasis and has been regarded as an anticancer herb in modern clinical practice. However, the anticancer effects and related molecular mechanisms of Curcuma aromatica remain unclear. In the present study, human colon carcinoma LS-174-T cell line with wild-type p53 was used as a model cell to evaluate the anticancer effects of aqueous extract of Curcuma aromatica (AECA). AECA inhibits LS-174-T cell proliferation in a dose- and time-dependent manner and colony formation in a dose-dependent manner. AECA treatment induces apoptosis accompanied by caspase-8, -9, and -3 activation in LS-174-T cells. Moreover, blocking the activities of these caspases with a specific inhibitor significantly protected LS-174-T cells from AECA-induced apoptosis. AECA treatment also induces G2/M phase arrest in LS-174-T cells. Expression of p53 was unchanged after AECA treatment; specific silence of p53 did not influence AECA-induced apoptosis and G2/M phase arrest. Further, the expression of cyclin B1 and CDK1 was reduced by AECA. This study suggests that AECA might be effective as an antiproliferative herb for colon carcinoma, the antitumor activity of AECA may involve both extrinsic and intrinsic apoptosis, and AECA induces G2/M phase arrest via downregulation of cyclin B1 and CDK1 and without the participation of p53.     

Growth-inhibitory effects of the astaxanthin-rich alga Haematococcus pluvialis in human colon cancer cells

The growth-inhibitory effects of the astaxanthin-rich Haematococcus pluvialis were studied in HCT-116 colon cancer cells. H. pluvialis extract (5–25 μg/ml) inhibited cell growth in a dose- and time-dependent manner, by arresting cell cycle progression and by promoting apoptosis. At 25 μg/ml of H. pluvialis extract, an increase of p53, p21^WAF-1/CIP-1 and p27 expression (220%, 160%, 250%, respectively) was observed, concomitantly with a decrease of cyclin D1 expression (58%) and AKT phosphorylation (21%). Moreover, the extract, at the same concentration, strongly up-regulated apoptosis by modifying the ratio of Bax/Bcl-2 and Bcl-XL, and increased the phosphorylation of p38, JNK, and ERK1/2 by 160%, 242%, 280%, respectively. Growth-inhibitory effects by H. pluvialis were also observed in HT-29, LS-174, WiDr, SW-480 cells. This study suggests that H. pluvialis may protect from colon cancer.     

The Effect of Curcumin on Proliferation and Apoptosis in LNCaP Prostate Cancer Cells

OBJECTIVE To observe the effect of curcumin on proliferation and apop-tosis in the prostate cancer LNCaP cell line. METHODS The AXSYMTM system luciferase method was used to examine the effect of various concentratious of curcumin on the content of prostate specific antigen (PSA) in prostate cancer LNCaP cells. A pGL3-PSA luciferase expression vector, containing 640 bp DNA of the PSA gene 5' -promoter region was constructed and transfected into the LNCaP cells with lipofectin. By measuring luciferase activity, the effect of 10 μmol/L, 20 μmol/L, 30 and 40 μmol/L curcumin on the promoter was studied. Effects on cell growth and apoptosis were analyzed by microscopy, the MTT colorimetric assay and flow cytometry. Western-blotting was used to measure expression of the androgen receptor (AR) in the LNCaP cells treated with different concentrations of curcumin. RESULTS The results showed that the expression of PSA was inhibited as curcumin reduced the activity of luciferase. Curcumin also caused a sigificant concentration-dependent decrease in AR expession measured by Western -blotting. Cell growth was inhibited and apoptosis was induced. CONCLUSION By inhibiting AR expression, curcumin reduced the function of the PSA promoter and inhibited PSA protein expression. Curcumin decreased the cellular proliferation and induced apoptosis in LNCaP cells in a concention-dependent manner.     

结肠腺癌细胞中eIF-4E调节NF-κB表达及对乙酰肝素酶转录表达和活性的影响

背景与目的：近期研究显示,人类肿瘤细胞部分转录因子可能受真核细胞起始因子-4E(eukaryotic initiation factor 4E,eIF-4E)在翻译水平上的调节,此关键转录因子表达水平的变化可从转录水平改变某些恶性相关基因产物的表达。本研究旨在探讨结肠腺癌LS-174T细胞中eIF-4E对转录因子NF-κB表达和活性的影响,并观察NF-κB活性水平对乙酰肝素酶基因转录的作用。方法：将与eIF-4E mRNA翻译起始区互补的反义寡核苷酸(antisense oligodeoxynucleotide,ASODN)经脂质体包裹后转染人结肠癌细胞LS-174T,以阻抑eIF-4E表达。随之使用Western blot和电泳迁移改变分析(electrophoretic mobility shift assays,EMSA)方法检测NF-κB蛋白表达量及活性水平。通过RT-PCR、Western blot方法观察乙酰肝素酶转录水平和蛋白表达量的改变;乙酰肝素酶活力采用特异酶活性检测方法,以放射性标记的硫酸乙酰肝素做为底物,凝胶过滤层析分离酶降解产物来分析。结果：针对eIF-4E的20个残基的ASODN经脂质体转染LS-174T细胞后,eIF-4E基因表达在转录和翻译水平都受到显著阻滞。eIF-4E基因阻抑表达引起结肠癌LS-174T细胞NF-κB蛋白表达量及其活性的显著下降;此外,转录因子NF-κB的下调也导致乙酰肝素酶基因的转录表达下降,并且被转染的肿瘤细胞在乙酰肝素酶的蛋白和活性表达水平上也显著下降。结论：结肠腺癌细胞LS-174T中eIF-4E在NF-κB的翻译调控中起重要作用。NF-κB作为调控乙酰肝素酶基因表达的重要转录因子,阻滞其活性将显著降低乙酰肝素酶基因的转录表达,并且其蛋白表达和酶活性水平也随之降低。     

真核细胞起始因子阻滞对LS-174T细胞乙酰肝素酶表达及活性的影响

目的 确定结肠癌细胞中真核细胞起始因子-4E(eukaryotic initiation factor-4E,eIF-4E)是否在帽依赖翻译水平上调控乙酰肝素酶的表达,并对乙酰肝素酶表达和肿瘤细胞侵袭性改变的相关性进行探讨。方法 采用Western blot和RT-PCR方法,分别检测eIF-4E被阻抑后其转录和翻译水平的改变。乙酰肝素酶活力是以其将大分子放射性元素(^35S)标记硫酸乙酰肝素底物降解为小分子的能力来确定。癌细胞侵袭力改变使用膜浸润培养系统来检测。结果 反义寡核苷酸(asODN)经脂质体转染LS-174T细胞后,eIF-4E基因表达明显抑制,其蛋白表达也显著下降。伴随eIF-4E被阻抑,LS-174T细胞乙酰肝素酶的活力和蛋白表达量均下降,并伴有癌细胞体外侵袭力的下降。结论 eIF-4E在翻译步骤对乙酰肝素酶表达具有调控作用,可作为调节乙酰肝素酶表达的治疗靶点。     

Flow cytometric identification of cell surface markers on cultured human colonic cell lines using monoclonal antibodies

Background. The expression of tumor-associated cell surface antigens is a reflection of the state of cell differentiation of tumor cells in culture. Method. Monoclonal antibodies (MoAbs) against the tumor-associated antigens carcinoembryonic antigen (CEA) and CA19-9 and the extracellular matrix protein CD44 were used to label the cell surface of human colonic cells in culture. The binding of each antibody to its respective antigen was measured by fluorescence-activated flow cytometry and expressed as a percentage of positive cells. Results. The human colon adenocarcinoma cell (HCAC) line, LS-180, showed strong binding with CEA (81%), CA 19-9 (87%), and CD44 (83%). LS-174t cells, a trypsinized variant of LS-180 cells, showed less binding with CEA (66%) and CA 19-9 (49%), but no binding with CD44. With cells from HCAC line HT-29, antigen expression was highly variable for CEA (13% ± 18) and CD44 (31% ± 35) but was consistently positive for CA19-9 (33% ± 13). The expression of CEA in the Caco-2 cell line was weak (24%), whereas there was no expression of CA19-9 and CD44. Normal human colon fibroblast cells (CCD-18Co) did not recognize the monoclonal antibodies to CEA or CA 19-9, but were strongly positive with the CD44 antibody (97%). Conclusions. These results support the concept that the expression of the tumor associated markers CEA and CA19-9 and the cell surface marker CD44 on human colonic cell lines varies with the degree of cellular differentiation. Carcinoembryonic antigen and/or CA19-9 were expressed in all four human colon adenocarcinoma cell lines, but not in the normal colon fibroblast cells (CCD-18Co). Using these two MoAbs appeared to be a more reliable measure of the state of differentiation of human colon adenocarcinoma cells. Cancer 1995; 75:195–200.     

PCNA的表达与人乳腺癌细胞凋亡的关系

目的：研究增殖细胞核抗原（PCNA）的表达与人乳腺癌细胞凋亡的关系。方法：以乳腺癌细胞株MCF-7／S（化疗敏感细胞株）为研究对象,应用MTT比色法检测阿霉素（ADR）对体外培养的MCF-7／S细胞增殖抑制作用,末端标记（TUNEL）法检测ADR诱导乳腺癌细胞凋亡,免疫细胞化学法检测ADR作用前后PCNA的表达。结果：ADR抑制MCF-7／S细胞增殖,旱剂量依赖性,IC50为0．128mg／L;ADR作用组MCF-7／S细胞的凋亡率（Apoptoticrate,AR）为0．261,与对照组细胞的凋亡率0．0449相比明显增高（P〈0．01）;PCNA阳性表达率为0．3371,与对照组PCNA阳性表达率0．5152相比明显降低（P〈0．01）。结论：乳腺癌肿瘤细胞的凋亡率（AR）和PCNA的阳性表达呈负相关;ADR能诱导MCF-7／S细胞凋亡,并能抑制其增殖。     

去甲斑蝥素对人胆囊癌GBC-SD细胞系增殖及侵袭的影响

目的　探讨去甲斑蝥素 (NCTD)对人胆囊癌GBC SD细胞系增殖、侵袭的影响及其机制。方法　应用细胞培养技术培养GBC SD细胞 ;以MTT法检测NCTD对GBC SD细胞的杀伤抑制率 ;以Matrigel侵袭实验、过河实验和SABC法检测NCTD对GBC SD细胞的侵袭力和对PCNA、Ki 6 7、MMP2 、TIMP2 蛋白表达的影响。结果　NCTD可明显抑制GBC SD细胞的增殖和生长 ,且随浓度提高或时间延长作用增强 ,呈剂量 时间效应关系 ;IC50 为 5 6 .18μg/ml,最强抑制作用时间为第 4 8小时。Matrigel侵袭、过河实验显示 ,NCTD在 5 μg/ml时 ,即能抑制GBC SD细胞的体外侵袭和运动能力 ,随浓度提高 ,过膜细胞减少 ,过膜死亡细胞增多 ,过河时间延长 (P <0 .0 1)。免疫组化测定显示 ,NCTD(IC50 )作用 4 8h后 ,GBC SD细胞PCNA、Ki 6 7、MMP2 表达下降 ,TIMP2 表达上升 ,MMP2 /TIMP2 比值下降 (P <0 .0 5 )。结论　NCTD可抑制人胆囊癌GBC SD细胞的生长 ,低浓度下也能抑制其体外侵袭能力 ;其机制可能与直接抑制GBC SD细胞迁移运动 ,干扰GBC SD细胞增殖相关基因蛋白PCNA、Ki 6 7和细胞基质溶解相关基因蛋白MMP2 、TIMP2 的表达有关。     

Effects of dietary zinc deficiency on esophageal squamous cell proliferation and the mechanisms involved

BACKGROUNDDietary zinc deficiency has been shown to be associated with the development of esophageal cancer in humans, but the exact mechanism of action is not knownAIMTo observe the effects of dietary zinc deficiency on esophageal squamous cell proliferation. METHODSThirty C57BL/6 mice were randomly divided into three groups: A zinc-sufficient (ZS) group, zinc-deficient (ZD) group, and zinc-replenished (ZR) group. For weeks 1–10, zinc levels in the mice diets were 30.66–30.89 mg/kg in the ZS group and 0.66–0.89 mg/kg in the ZD and ZR groups. During weeks 10–12, the ZR group was switched to the ZS diet; the other two groups had no changes in their diets. Changes in body weight, serum, and esophageal tissue zinc concentrations were assessed as well as differences in the expression of proliferating cell nuclear antigen (PCNA), mitogen-activated protein kinase p38 (p38MAPK), nuclear factor kappa B (NF-κB) p105, NF-κB p65, and cyclooxygenase (COX)-2 proteins in the esophageal mucosa.RESULTSThe body weight and zinc concentration in the serum and esophageal mucosa were significantly lower in the ZD and ZR groups than in the ZS group (P < 0.05). In ZD mice, there was a marked proliferation of basal cells in the esophageal mucosa, resulting in a disturbance in the arrangement of basal cells in layers 2–4, a thickening of the squamous layer, and a significant increase in the expression of the above-mentioned five proteins involved in proliferation and inflammation in the esophageal mucosa. Two weeks after switching to the ZS diet, the serum zinc concentration in the ZR group increased, and the expression of PCNA, NF-κB p105, and COX-2 decreased, but the concentration of zinc in the esophageal mucosa and the structure of the esophageal mucosa did not display any significant changesCONCLUSIONThe ZD diet decreased the growth rate and promoted the proliferation of esophageal squamous cells in mice. The mechanism of proliferation was related to the induced overexpression of COX-2, P38, PCNA, and NF-κB (p105 and p65), and the ZR diet reduced the expression of PCNA, NF-κB p105, and COX-2, thereby reversing this process.​     

西黄浸提液抑制胃癌SGC-7901 细胞增殖的可能机制

[摘要] 目的：探讨西黄浸提液对胃癌SGC-7901 细胞增殖的影响及其可能机制。方法：常规培养胃癌细胞株SGC-7901,用CCK-8 法和细胞流式细胞术检测不同质量浓度（3.2、6.4、12.8 和25.6 mg/ml）的西黄浸提液在不同时间点（24、48 和72 h）对SGC-7901 细胞增殖和凋亡的影响,用qPCR法检测不同质量浓度西黄浸提液对SGC-7901 细胞凋亡相关基因Bax 和Bcl-2 mRNA表达的影响,用Western blotting 检测西黄浸提液对凋亡相关蛋白caspase 3、caspase 9、Bax和Bcl-2 表达的影响。结果：3.2~25.6 mg/ml的西黄浸提液均能有效地抑制胃癌SGC-7901 细胞的增殖（P<0.05 或P<0.01）,并且随浓度增加SGC-7901 细胞凋亡率增加（P<0.01）。西黄浸提液能够显著上调SGC-7901 细胞Bax mRNA和下调Bcl-2 mRNA表达水平（P<0.05 或P<0.01）,并可增加caspase3、caspase 9 和Bax 蛋白表达、降低Bcl-2 蛋白表达（P<0.05 或P<0.01）。结论：西黄浸提液通过触发细胞凋亡抑制胃癌SGC-7901细胞的增殖,此可成为一个潜在的胃癌辅助治疗的方法。     

膜联蛋白A7低表达对胃癌MGC-803细胞增殖和凋亡的影响

目的:探讨RNA干扰技术靶向沉默膜联蛋白A7(anexin A7,ANXA7)的表达对人胃癌MGC-803细胞增殖和凋亡的影响。方法:实验分为3组,以靶向ANXA7的siRNA转染MGC-803细胞为siRNA干扰组,另设阴性siRNA对照和空白对照组。Western blotting检测转染后MGC-803细胞中ANXA7蛋白的表达,应用MTT、集落形成和流式细胞术检测ANXA7下调对MGC-803细胞增殖、凋亡的影响。结果:靶向ANXA7的siRNA转染后MGC-803细胞中ANXA7的表达较阴性对照和空白对照组细胞明显降低[(21.79±1.72)%vs(99.87±5.13)%、(93.45±4.89)%,均P<0.05]。下调ANXA7明显降低MGC-803细胞的增殖能力[(0.97±0.06)vs(1.21±0.07)、(1.25±0.08),均P<0.05]和集落形成能力[(183±21)vs(363±35)、(348±27)个,均P<0.05],细胞凋亡率无显著变化(P>0.05)。结论:ANXA7低表达可抑制胃癌细胞MGC-803增殖,而对细胞凋亡无明显影响。     

Betaine Effects on Morphology,Proliferation, and p53-induced Apoptosis of HeLa Cervical Carcinoma Cells in Vitro

Objectives: To investigate the effects of betaine on HeLa cell growth and apoptosis and molecular mechanisms.Materials and Methods: Concentrations of 0.1, 1.0, 5.0, 20.0, 100.0 mg/ml of betaine were used to evaluate theanticancer efficacy for HeLa cells respectively, and MCF-10A was also detected as a normal diploid cell control.Results: We found that proliferation of HeLa cells was inhibited significantly upon exposure to increasing betainelevels with the MTT test (p<0.05). The percentage of S phase cells in the low dose groups (< 5mg/ml) were distinctlyhigher than in high dose groups, and the rates of Sub-G1 phase were the opposite (p<0.01); A high concentrationof betaine (>5.0mg/ml) significantly promoted the apoptosis of HeLa cells (p<0.01). SOD activities of the lowdose groups were slightly higher than the control group (p<0.05) and there were obvious synchronicity andcorrelation among the expression of promoting apoptosis genes Bax, P53, Caspase 3 and apoptosis suppressiongene Bcl-2. In response to an apoptosis-inducing stimulus, p53 and cyclin D1 could be activated with blockageof the cell cycle at G1/S or S/G2 checkpoints. Conclusions: Our data showed that betaine could promote HeLacells proliferation in vitro at low concentrations.In contrast, high concentrations could significantly inhibit cellgrowth and migration, and induce apoptosis of HeLa cells through caspase 3 signaling and further promotednecrosis. This might imply that betaine exhibits tumoricidal effects and acts as a biological response modifier incancer treatment by inducing apoptosis and cell cycle arrest in a dose and time-dependent manner.     

As4S4 Induced Apoptosis in HeLa Cells and Its Molecular Mechanism

Objective To investigate the As4S4 induced growth inhibition and apoptosis in HeLa cells and its possible relationship with cyclooxygenase-2 (COX-2). Methods HeLa cells were treated with various concentrations (7.5, 15, 30, 60 mg/L) of As4S4 at different times (12, 24, 36, 48, 60 h). Cell growth was measured by MTT. Apoptosis was detected by double staining flow cytometry (FCM). Levels of PGE2 were measured by radioimmunoassay. The expression of COX-2 protein was examined by Western blot analysis. Results After treated with different concentrations of As4S4, the growth of HeLa cells was suppressed significantly in a dose-and time-dependent manner. The IC50 of 24 h was 30 mg/L (P＜0.01). As4S4 induced apoptosis with apoptosis rates at 8.13%-62.36% by flow cytometry (FCM) in a dose-dependent manners. The release of PGE2 was reduced in HeLa cells with the values being (70.56±2.03), (48.58±2.28), (29.25±1.57) and (18.02±1.04) respectively, significantly different compared with control group (3.15±0.01) (P＜0.01). As4S4 also inhibited the activity and expression of COX-2 in a dose dependent manner and down-regulated the expression of COX-2 protein greatly. Conclusion As4S4 could inhibit the proliferation and increase apoptosis in human HeLa cells. These effects may depend on the inhibition of the expression of COX-2 and PGE2 by As4S4.     

苹果多酚通过激活AMPK/SIRT1信号通路对LPS诱导的肺上皮细胞自噬反应的影响

目的:探讨苹果多酚通过调节腺苷酸活化蛋白激酶/沉默信息调节因子1（AMP-activated protein kinase/Sirtuin1,AMPK/SIRT1)信号通路对脂多糖（lipopolysaccharide,LPS）诱导的人肺泡上皮细胞（A549）自噬反应的影响。方法:使用不同浓度的苹果多酚提取物（apple polyphenol extract,APE）预处理A549细胞2 h后,LPS诱导A549细胞培养24 h,MTT法检测增殖活性,筛选APE最佳预处理浓度;将A549细胞分为对照组、LPS组（3 mg/L LPS）、LPS+APE组（3 mg/L LPS+20 μg/mL APE）、APE+Compound C组（3 mg/L LPS+20 μg/mL APE+50 μmol/L Compound C）,免疫荧光染色观察A549细胞自噬;流式细胞术检测A549细胞凋亡;Western blot法检测细胞中自噬相关蛋白及AMPK/SIRT1通路相关蛋白表达水平。结果:与对照组比较,经LPS诱导的A549细胞增殖活性、自噬水平、LC3Ⅱ/LC3Ⅰ、Beclin-1、SIRT1、p-ULK1/ULK1、p-AMPK/AMPK蛋白表达降低,p62蛋白表达及细胞凋亡率升高（P＜0.05）;与LPS组比较,LPS+APE组细胞增殖活性、自噬水平、LC3Ⅱ/LC3Ⅰ、Beclin-1、SIRT1、p-ULK1/ULK1、p-AMPK/AMPK蛋白表达水平显著升高,p62蛋白表达及细胞凋亡率显著降低（P＜0.05）;与LPS+APE组比较,APE+Compound C组A549细胞增殖活性、自噬水平、LC3Ⅱ/LC3Ⅰ、Beclin-1、SIRT1、p-ULK1/ULK1、p-AMPK/AMPK蛋白表达水平显著降低,p62蛋白表达及细胞凋亡率显著升高（P＜0.05）。结论:苹果多酚通过激活AMPK/SIRT1 信号通路提高LPS诱导的肺上皮细胞自噬,降低细胞凋亡。