溶血磷脂酸抑制顺铂诱导的卵巢癌细胞凋亡

目的：探讨溶血磷脂酸（lysophosphatidic acid,LPA）对顺铂诱导的卵巢癌细胞凋亡的抑制作用及其作用机制。方法：体外培养卵巢癌细胞株SKOV3,采用MTT法检测LPA对顺铂（cisplatin,DDP）作用后卵巢癌细胞株SKOV3增殖活性的影响,Hoechst33258荧光染色观察凋亡细胞,用FCM法分析细胞周期变化和细胞凋亡率,DNA片段凝胶电泳观察凋亡细胞的DNA“梯状”条带,免疫细胞化学法及RT-PCR法分别检测细胞凋亡相关蛋白及其mRNA的表达。结果：LPA能降低DDP对SKOV3细胞生长的抑制作用,同时增加G0/G1期细胞比例,降低S期细胞比例和凋亡率。Hoechst33258染色检测示LPA作用后凋亡小体明显减少。DNA片段凝胶电泳示LPA作用后不产生明显的凋亡片段。10μmol/L的LPA作用SKOV3细胞48h后,bcl-2基因及其蛋白表达水平升高,而bax基因及其蛋白表达水平降低（P〈0.01）。结论：LPA可通过上调bcl-2基因及蛋白表达,下调bax基因及蛋白表达,抑制DDP诱导的卵巢癌细胞凋亡。因此,针对LPA的治疗有望提高DDP疗效,改善卵巢癌患者的预后。     

Induction of apoptosis in human ovarian epithelial cancer cells by antisurvivin oligonucleotides

Survivin, an anti-apoptosis gene that is abnormally overexpressed in a variety of human tumors, may play an important role in the carcinogenesis and drug resistance of cancer. This study was designed to explore the effects of liposome-survivin antisense oligonucleotide (Lip-ASODN) on the growth and apoptosis of human ovarian cancer cell lines, A2780 and SKOV3. To investigate the use of survivin as a therapeutic target on ovarian cancer, we carried out transfections with Lip-ASODN to induce apoptosis in ovarian cancer cell lines, A2780 and SKOV3. The expression of survivin mRNA and relative protein were evaluated separately by quantitative real-time RT-PCR and Western blot analysis. Cell proliferation inhibition was determined by methyl thiazolyl tetrazolium (MTT) assay, and the induced cell apoptosis was examined using flow cytometry (FCM) after Lip-ASODN transfection. Our results showed that the overexpression of survivin led to infinite carcino-proliferation, and survivin expression in the survivin-positive ovarian cancer cell line A2780 and SKOV3 cells was significantly and gradually reduced when transfected with Lip-ASODN at concentrations of 200, 400 and 600 nM by degrees. Lip-ASODN transfection induced greater apoptosis rates in the human ovarian cancer cell lines A2780 and SKOV3 (p<0.05). The growth inhibition and apoptotic rates of tumor cells change when treated with different concentrations of Lip-ASODN. The cell growth inhibition peak rate was reached when increasing Lip-ASODN concentration to 600 nM. Furthermore, time course evaluation showed that survivin protein expression was inhibited by Lip-ASODN within 12 h after transfection. We concluded that down-regulation of survivin by a targeted antisense oligonucleotide appears to be an effective gene therapy approach in the treatment of ovarian cancer.     

The proliferation,apoptosis, invasion of endothelial-like epithelial ovarian cancer cells induced by hypoxia

Background

Epithelial ovarian cancer is one of the most malignant cancers in women because metastasis occurs in the most of patients by the time of diagnosis. Cancer cells have strong capacity to form angiogenesis or vasculogenic mimicry, which plays the major role in its malignant phenotype. Vasculogenic mimicry might contribute to the failure of the angiogenesis-targeted therapy strategies. Under the microenvironment of the tumor, hypoxia is the most common phenomena because of the vast energy and oxygen consuming. In the present study, the endothelial-like cells induced by hypoxia from SKOV-3 and ES-2 ovarian cancer cells were harvested to investigate the changes in their biological behaviors.

Methods

The endothelial-like cells from SKOV-3 and ES-2 cells were harvested by laser capture microdissection. The biological behaviors of the endothelial-like cells, including proliferation, cell cycle, apoptosis, invasion and telomerase activity were determined by MTT, FCM, Transwell chamber and TRAP-ELISA methods. HIF-1α is the most important factor for the behavior changes under hypoxic condition. Some other genes relative to biological behaviors are also changes following the changes of HIF-1α. In order to elucidate the underlying mechanisms for these changes by hypoxia, the relative genes expressions including HIF-1α, CyclinD1, Flk-1, VEGF, p53 and V-src were determined by real-time PCR.

Results

SKOV-3 and ES-2 cells were resistant to hypoxia by adoption of proliferation, apoptosis, differentiation and invasion. Combined with other studies, the more poorly cancer cells differentiate, the more strongly cells are resistant to hypoxia, the more possible to form vasculogenic mimicry. The changes in the expression of HIF-1α, and HIF-1α-dependent VEGF, Flk-1, Cyclin D1, and HIF-1α-independent p53 have been involved in this process.

Conclusions

HIF-1α took an important role in the behavioral changes of SKOV-3 and ES-2 cells by hypoxia. At the same time, other mechanisms were also involved in this process.     

12-Lipoxygenase inhibition induced apoptosis in human gastric cancer cells

Arachidonic acid release from membrane phospholipids is essential for tumour cell proliferation. Lipoxygenases constitute a pathway for arachidonate metabolism. The present study investigated the expression of 12-lipoxygenase and its effect on cell proliferation as well as survival in two human gastric cancer cell lines (AGS and MKN-28). RT-PCR and western blots, respectively, showed 12-LOX mRNA and protein expression in both AGS and MKN-28 cell lines. Treatment with a 12-LOX inhibitor, baicalein, significantly inhibited cancer cell proliferation, but a metabolite of 12-LOX activity, 12 hydroxyeicosatetraenoic acid (12-HETE) reversed baicalein-induced growth inhibition. Furthermore, the blockade of the 12-LOX pathway through a 12-LOX inhibitor and antisense induced apoptosis of gastric cancer cell lines. The biochemical characteristics of apoptosis were p53-independent combined with a decrease in bcl-2 expression. Caspase-7 was proteolytically activated and responsible for the apoptosis execution.     

GRP78在蛋白酶体抑制剂诱导甲状腺癌细胞凋亡中的作用

目的:探讨葡萄糖调节蛋白78(GRP78)在蛋白酶体抑制剂诱导甲状腺癌细胞凋亡中的作用.方法:对2种人甲状腺未分化癌细胞系FRO、AR0分别设空白对照组和蛋白酶体抑制荆处理组;及siGRP78、随机序列核酸siRNA和错位型siGRP78组.利用蛋白酶体抑制荆MG132(1μtmol/L)、PSI(10 nmol/L)和EPOX(5 nmol/L)作用2种细胞系,实时定量RT-PCR和蛋白质印迹法检测各组细胞GRP78 mRNA、蛋白表达.流式细胞仪检测细胞凋亡.结果:蛋白酶体抑制剂处理24 h后,2种细胞系中GRP78mRNA及蛋白水平保持相似增长高峰,为空白对照组2～3倍(P<0.01);siGRP78转染24 h,细胞总GRP78 mRNA丢失>80%,转染48 h,GRP78蛋白总量丢失>75%.蛋白酶体抑制剂MG132作用后,ARO、FRO细胞凋亡率分别为8.3%和78.3%;当siGRP78靶向沉默GRP78后,蛋白酶体抑制剂诱导2种细胞凋亡率显著增加,AR0细胞凋亡率提高5倍左右(P<0.01).结论:2种甲状腺癌细胞系存在GRP78基因表达,不同程度干扰蛋白酶体抑制荆凋亡诱导作用;沉默GRP78基因表达可提高蛋白酶体抑制荆对肿瘤细胞杀伤率.     

Overexpression of Bax sensitizes human pancreatic cancer cells to apoptosis induced by chemotherapeutic agents

PURPOSE: Bax plays an important role in the regulation of apoptosis induced by chemotherapy and other stimuli. We therefore investigated the role of Bax in drug-induced apoptosis in human pancreatic cancer cells. METHOD: A tetracycline-inducible retroviral expression vector bearing the human bax-alpha gene was constructed. ASPC-1 cells were stably infected with this vector. The sensitivity of the transformed cell line to gemcitabine and 5-Fu was assessed. RESULTS: Western blots revealed that Bax expression was enhanced in these cells by the tetracycline analogue doxycycline. Enhanced expression of Bax itself did not inhibit the growth rate of infected cells and did not influence expression of Bcl-2 and Bcl-xL. However, it significantly increased the sensitivity of cells to the chemotherapeutic drugs gemcitabine and 5-Fu. These drugs also activated caspase-8 and caspase-3 by up to ninefold. Caspase activation and/or an imbalance in Bax and Bcl-2/Bcl-xL expression may be the reasons for the augmentation of cytotoxicity by these drugs. CONCLUSIONS: The findings suggest that enhanced Bax expression may have therapeutic application in enhancing the efficacy of chemotherapy in pancreatic cancers.     

Precancerous model of human breast epithelial cells induced by NNK for prevention

Epidemiological investigations have suggested that exposure to tobacco and environmental carcinogens increase the risk of developing human breast cancer. In light of the chronic exposure of human breast tissues to tobacco and environmental carcinogens, we have taken an approach of analyzing cellular changes of immortalized non-cancerous human breast epithelial MCF10A cells during the acquisition of cancerous properties induced by repeated exposure to the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) at a low concentration of 100 pM. We found that accumulated exposures of MCF10A cells to NNK result in progressive development of cellular carcinogenesis from a stage of immortalization to precancerous sub-stages of acquiring a reduced dependence on growth factors and acquiring anchorage-independent growth. Using Matrigel for MCF10A cells to form size-restricted acini, we detected that exposures to NNK resulted in altered acinar conformation. Analysis of gene expression profiles by cDNA microarrays revealed up- and down-regulated genes associated with NNK-induced carcinogenesis. Using this cellular carcinogenesis model as a target system to identify anticancer agents, we detected that grape seed proanthocyanadin extract significantly suppressed NNK-induced carcinogenesis of MCF10A cells. Our studies provide a carcinogenesis-cellular model mimicking the accumulative exposure to carcinogens in the progression of human breast epithelial cells to increasingly acquire cancerous properties, as likely occurs in the development of precancerous human breast cells. Our cellular model also serves as a cost-efficient, in vitro system to identify preventive agents that inhibit human breast cell carcinogenesis induced by chronic exposures to carcinogens.     

紫杉醇诱导子宫颈癌H eLa细胞自噬性凋亡的观察

目的观察紫杉醇对体外培养的子宫颈癌HeLa细胞自噬性凋亡的影响,并初步探讨其可能的机制。方法不同浓度（1.2、6、12、24、36 mg/L）的紫杉醇处理体外子宫颈癌HeLa细胞6、12、24、48、72小时后,用MTT法测定其生长抑制率,倒置显微镜及透视电镜观察细胞形态学变化,通过流式细胞术分别测定细胞凋亡率、细胞周期分布,RT-PCR检测自噬基因Beclin1表达的变化情况。结果紫杉醇呈剂量和时间依赖性抑制子宫颈癌HeLa细胞增殖;紫杉醇12 mg/L处理的HeLa细胞,早期（24小时内）可出现明显的细胞自噬性变化,细胞凋亡数明显增加,G2/M期阻滞,且自噬基因Beclin1的表达明显增高。结论紫杉醇具有抑制子宫颈癌HeLa细胞增殖、诱导细胞自噬性凋亡等作用,诱导子宫颈癌HeLa细胞发生自噬性凋亡,其机制可能与上调自噬基因Beclin1的表达水平有关。     

Hypoxia increases resistance of human pancreatic cancer cells to apoptosis induced by gemcitabine.

PURPOSE: Hypoxia, frequently found in the center of solid tumor, is associated with resistance to chemotherapy by activation of signaling pathways that regulate cell pro-liferation, angiogenesis, and apoptosis. We determined whether hypoxia can increase the resistance of human pancreatic carcinoma cells to gemcitabine-induced apoptosis by activation of phosphatidylinositol 3'-kinase (PI3K)/Akt, MEK/mitogen-activated protein kinase (extracellular signal-regulated kinase) [MAPK(Erk) kinase (MEK)], and nuclear factor kappa B (NF-kappa B) signaling pathways. EXPERIMENTAL DESIGN: We evaluated the phosphorylation of Akt and MAPK(Erk), DNA binding activity of NF-kappa B, and apoptosis induced by gemcitabine in L3.6pl human pancreatic cancer cells under normoxic and hypoxic conditions. We then examined the effects of the PI3K inhibitor LY294002, MEK inhibitor U0126, and the epidermal growth factor receptor tyrosine kinase inhibitor PKI 166 on these signaling pathways and induction of apoptosis. RESULTS: Hypoxic conditions increased phosphorylation of Akt and MAPK(Erk) and NF-kappa B DNA binding activity in L3.6pl cells. The activation of Akt and NF-kappa B was prevented by LY294002, whereas the activity of MAPK(Erk), but not NF-kappa B, was inhibited by U0126. The increased activation of Akt, NF-kappa B, and MAPK(Erk) was inhibited by PKI 166. Under hypoxic conditions, L3.6pl cells were resistant to apoptosis induced by gemcitabine. The addition of LY294002 or PKI 166 abrogated cell resistance to gemcitabine, whereas U0126 only partially decreased this resistance. CONCLUSIONS: These data demonstrate that hypoxia can induce resistance of pancreatic cancer cells to gemcitabine mainly through the PI3K/Akt/NF-kappa B pathways and partially through the MAPK(Erk) signaling pathway. Because PKI 166 prevented the activation of PI3K/Akt/NF-kappa B and MAPK(Erk) pathways, the combination of this tyrosine kinase inhibitor with gemcitabine should be an effective therapy for pancreatic cancer.     

Implication of multiple mechanisms in apoptosis induced by the synthetic retinoid CD437 in human prostate carcinoma cells

The synthetic retinoid 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid (CD437) induces apoptosis in several types of cancer cell. CD437 inhibited the growth of both androgen-dependent and -independent human prostate carcinoma (HPC) cells in a concentration-dependent manner by rapid induction of apoptosis. CD437 was more effective in killing androgen-independent HPC cells such as DU145 and PC-3 than the androgen-dependent LNCaP cells. The caspase inhibitors Z-VAD-FMK and Z-DEVD-FMK blocked apoptosis induced by CD437 in DU145 and LNCaP cells, in which increased caspase-3 activity and PARP cleavage were observed, but not in PC-3 cells, in which CD437 did not induce caspase-3 activation and PARP cleavage. Thus, CD437 can induce either caspase-dependent or caspase-independent apoptosis in HPC cells. CD437 increased the expression of c-Myc, c-Jun, c-Fos, and death receptors DR4, DR5 and Fas. CD437's potency in apoptosis induction in the different cell lines was correlated with its effects on the expression of oncogenes and death receptors, thus implicating these genes in CD437-induced apoptosis in HPC cells. However, the importance and contribution of each of these genes in different HPC cell lines may vary. Because CD437 induced the expression of DR4, DR5 and Fas, we examined the effects of combining CD437 and tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and Fas ligand, respectively, in HPC cells. We found synergistic induction of apoptosis, highlighting the importance of the modulation of these death receptors in CD437-induced apoptosis in HPC cells. This result also suggests a potential strategy of using CD437 with TRAIL for treatment of HPC. Oncogene (2000) 19, 4513 - 4522.     

姜黄素诱导人胃癌细胞SGC-7901凋亡的作用机制

 目的 探讨姜黄素诱导人胃癌细胞SGC-7901凋亡的作用及其相关机制。方法 以不同浓度的姜黄素作用于胃癌SGC-7901细胞，利用倒置相差显微镜观察细胞生长形态变化，通过MTT检测细胞生长抑制率，流式细胞术检测细胞凋亡，Western blot 检测胃癌细胞中Fas及survivin的表达情况。结果 姜黄素能显著抑制体外培养的SGC-7901细胞的生长并呈量-效和时-效关系，流式细胞术检测到亚二倍体凋亡峰，细胞凋亡率增加，Western blot结果提示经姜黄素作用后Fas表达率上升，survivin表达率下降。结论 姜黄素能抑制胃癌细胞SGC-7901的生长并促进其凋亡，姜黄素可能通过上调Fas及下调survivin的表达而诱导凋亡。     

Induction of apoptosis in human lung cancer cells by curcumin

Curcumin, a phenolic compound from the rhizome of the plant Curcuma longa has anti-inflammatory, antioxidant and anti-cancer activities. Although the precise mode of action of this compound is not yet elucidated, studies have shown that chemo-preventive action of curcumin might be due to its ability to induce apoptosis and to arrest cell cycle. This study investigated the cellular and molecular changes induced by curcumin leading to the induction of apoptosis in human lung cancer cell lines-A549 and H1299. A549 is p53 proficient and H1299 is p53 null mutant. The lung cancer cells were treated with curcumin (0-160 microM) for 12-72 h. Curcumin inhibited the growth of both the cell lines in a concentration dependent manner. Growth inhibition of H1299 cell lines was both time and concentration dependent. Curcumin induced apoptosis in both the lung cancer cell lines. A decrease in expression of p53, bcl-2, and bcl-X(L) was observed after 12 h exposure of 40 microM curcumin. Bak and Caspase genes remained unchanged up to 60 microM curcumin but showed decrease in expression levels at 80-160 microM. The data also suggest a p53 independent induction of apoptosis in lung cancer cells.     

The multistage process of carcinogenesis in human esophageal epithelial cells induced by human papillomavirus

To investigate the multistage process of carcinogenesis, the progressive alteration of the morphology, telomerase, cytogenesis, oncogenes and tumorigenicity in the process of immortalization and malignant transformation of the human fetal esophageal epithelial cell (SHEE) was studied. The SHEE cells were immortalized by gene E6E7 of human papilloma virus (HPV) type 18 in our laboratory and continually cultivated over 100 passages, which had been malignantly transformed. Cells at the 11th, 35th, 65th and 100th passage were examined according to the following criteria: morphological changes of cell growth, contact-inhibition and anchorage-independent growth (AIG); the cell proliferative and apoptotic index; the modal number of chromosomes; c-myc, p53, bcl-2, ras; telomere length and activities of telomerase and tumorigenicity in nude mice or severe combined immunodeficient (SCID) mice. The cells of the 11th passage were well differentiated and the cells of 100th passage were relatively poorly differentiated with polymorphism, while the cells of 35th and 65th had two distinct differentiations. The proliferative indexes were 21.1%, 32.5%, 33.2%, and 40.9% and the apoptotic indexes were 3.3%, 2.7%, 3.5%, 2.7% in the 11th, 35th, 65th and 100th passage respectively. Karyotypes of four cell passages belonged to hyperdiploidy and hypotriploidy. C-myc, ras, p53 genes were low in the 10th and 35th, and high in the 65th and 100th passage, but bcl-2 was low in 4 passages. Telomere length sharply decreased from normal fetal esophagus cells until the 35th passage, but it was stably expressed in the 65th and 100th passage. The activities of telomerase were expressed in cells of the 35th, 65th and 100th passages. The efficiency of AIG varied in different passages of the SHEE cell and was absent in the 11th passage, low efficiency in the 35th passage and 65th passage, and high efficiency in the 100th passage. Transplanted cells of the 65th and 100th passage into SCID mice resulted in tumor formation, but only the 100th passage cells could grow in nude mice. All of these characteristic changes were in dynamic progressive process. These data demonstrate that carcinogenesis of esophageal epithelial cells induced by HPV is the multistage process, which goes through the initial, immortal, premalignant and malignant transformation stages. The generation of esophageal carcinoma is caused by the accumulation of cellular, genetic and molecular changes.     

维生素E琥珀酸酯诱导MDA-MB-435乳腺癌细胞的凋亡

目的:检测维生素E琥珀酸酯(vitaminEsuccinate,VES)对MDAMB435乳腺癌细胞增殖抑制和凋亡诱导作用并分析凋亡诱导分子Fas表达的变化。方法:以VES刺激人乳腺癌细胞MDAMB435(雌激素受体阴性)12、24和48h,VES浓度为5、10和20μg/mL,以MTT法测定对细胞增殖的抑制作用,以流式细胞仪分析细胞周期和细胞表面Fas表达,TUNEL法检测肿瘤细胞凋亡指数变化,Westernblot法检测VES作用后Fas蛋白水平变化。结果:VES对MDAMB435乳腺癌细胞增殖具有显著的抑制作用并表现为时间和剂量依赖关系。流式细胞仪分析细胞凋亡,MDAMB435细胞的自然凋亡率为1.5%,5、10和20μg/mLVES分别作用48h后凋亡率升高至13.1%、20.2%和46.5%。TUNEL法检测VES作用后乳腺癌细胞凋亡指数由1.1±0.4升高至10.8±1.0、30.4±2.7和51.4±4.7,细胞Fas蛋白水平分别升高1.3、1.9和4.3倍,细胞表面Fas平均荧光强度由46.29升高至59.66、84.54和103.41。结论:VES对MDAMB435乳腺癌细胞具有显著的增殖抑制作用,并诱导细胞的凋亡,其机制与细胞表面Fas表达上调有关。     

白藜芦醇对脂多糖诱导的人肺泡上皮细胞A549凋亡的保护作用机制

目的:探讨白藜芦醇对脂多糖（lipopolysaccharide,LPS）诱导的人肺泡上皮细胞A549增殖、凋亡的影响。方法:用MTT法检测LPS对A549细胞增殖的影响;流式细胞仪检测细胞凋亡;Western blot检测凋亡相关信号通路蛋白的表达水平;实时荧光定量PCR和免疫荧光法分别在mRNA和蛋白水平检测其表达情况。结果:LPS能够以浓度梯度和时间梯度依赖的方式显著诱导肺癌细胞A549的凋亡,同时LPS能够升高细胞内活性氧的水平。Western blot结果表明LPS能够增加细胞内p53的表达水平并降低Bcl-2的表达。用白藜芦醇处理48h后,LPS所引起的细胞内活性氧水平升高的现象显著下降。Western blot结果表明白藜芦醇能够有效逆转LPS所引起的细胞内p53表达水平升高以及Bcl-2表达下降的情况。结论:白藜芦醇通过降低细胞内活性氧、p53水平以及升高Bcl-2水平对LPS所诱导的人肺泡上皮细胞A549凋亡起到保护作用。     

Curcumin in combination with bortezomib synergistically induced apoptosis in human multiple myeloma U266 cells

Growth of multiple myeloma cells is controlled by various factors derived from host bone marrow microenvironments. Interaction between multiple myeloma cells and bone marrow stromal cells (BMSCs) plays an important role in the expression of adhesive molecules and secretion of growth factors involved in multiple myeloma (MM) cell growth, survival, and resistance to anticancer drugs. Recently, the possibility of developing novel anti-cancer therapeutic strategies targeting both MM cells and MM cell–BMSC interactions has been discussed. Here we present data showing that curcumin, a major constituent of turmeric compounds extracted from the rhizomes of the plant Curcuma longa, effectively reduced the growth of MM cells and BMSCs. Upon treatment with curcumin, IL-6/sIL-6R-induced STAT3 and Erk phosphorylation was dramatically reduced in the co-cultured cells. In addition, curcumin inhibited the production of pro-inflammatory cytokines and VEGF, factors that are associated with the progression of multiple myeloma, from both MM cells and BMSCs. In a combination treatment with curcumin and bortezomib, IL-6/sIL-6R-induced STAT3 and Erk phosphorylation was effectively inhibited. Moreover, this combination treatment synergistically inhibited the growth of MM cells co-cultured with BMSCs as compared to controls. Taken together, these results indicate that curcumin potentiates the therapeutic efficacy of bortezomib in MM suggesting this combination therapy to be of value in the clinical management of MM.     

姜黄素对人肺癌A549细胞凋亡及细胞微丝骨架改变影响的研究

目的:观察姜黄素对人肺癌A549细胞凋亡的诱导作用及凋亡细胞骨架的改变。方法:选用不同剂量的姜黄素处理A549细胞,应用MTT法、透射电镜、FCM法检测姜黄素对细胞生长影响及对凋亡的诱导作用。应用荧光染色在激光共聚焦显微镜下观察凋亡细胞微丝的结构。结果:MTT法显示姜黄素抑制A549细胞的生长,具有时间和剂量的效应关系。FCM法显示,>10μmol/L浓度姜黄素作用24h后可诱导细胞凋亡,并出现凋亡峰(亚二倍体峰)。透射电镜观察发现,20μmol/L姜黄素作用24h后细胞数明显减少,并出现典型的凋亡形态。激光共聚焦显微镜观察显示,在细胞凋亡过程中,F-肌动蛋白(F-actin)发生聚集和重排,并出现细胞内F-actin含量逐渐减少。结论:姜黄素对人肺癌A549细胞具有抑制生长及诱导凋亡的作用,微丝的改变在凋亡形态变化中起着重要的作用。