冬凌草甲素诱导人肺腺癌细胞株A549凋亡及其机制研究

目的:探讨冬凌草甲素(oridnin)对人肺腺癌细胞株A549细胞凋亡的影响。方法:利用MTT法检测oridnin对A549细胞增殖作用的影响;Hoechst33258染色观察给药后细胞形态改变;透射电镜观察给药后细胞超微结构改变;FITC-Annexin V/PI双标记检测细胞凋亡率。结果:Hoechst33258染色和透射电镜观察,oridonin给药后A549细胞出现空泡变性,染色质高度凝集;FITC-AnnexinV/PI双标记检测oridnin(25,50,100μmol/L)作用细胞48h后凋亡率分别为1.5%,6.2%,59.7%。结论:Oridonin对A549细胞具有抑制增殖和诱导凋亡作用。     

紫花牡荆素诱导人肺腺癌A549细胞凋亡及其机制的探讨

目的探讨紫花牡荆素（CAS）诱导人肺腺癌A549细胞凋亡及其机制。方法平皿集落法测定CAS对A549细胞生长的抑制作用;碘化丙啶（PI）染色流式细胞术（FCM）分析细胞凋亡率;丫啶橙／溴乙啶（AO／EB）荧光染色观察细胞凋亡形态;Westernblot检测FoxMl（forkhead box protein M1）表达水平。结果CAS能抑制人肺腺癌A549细胞生长,呈浓度依赖性,半数抑制浓度（IC50）值为7．26p．mol·L^-1;CAS处理后A549细胞呈典型凋亡细胞形态学改变,诱导细胞凋亡呈浓度依赖性;CAS诱导A549细胞FoxM1蛋白表达下调,呈浓度和时间依赖性。结论CAS抑制人肺腺癌A549细胞的生长并诱导其凋亡,其作用机制可能与FoxM1表达下调有关。     

GSH 耗竭介导5, 7- 二甲氧基黄酮诱导肺癌A 549 细胞凋亡

目的探讨5,7-二甲氧基黄酮（5,7-dimethoxyflavone,DMF）诱导人肺癌A549细胞凋亡作用是否涉及细胞内谷胱甘肽（glutathione,GSH）耗竭。方法体外培养A549细胞,分光光度法测定细胞内GSH含量;流式细胞术检测细胞凋亡率;琼脂糖凝胶电泳观察细胞DNA断裂。结果 DMF以浓度依赖方式诱导A549细胞凋亡率增高（P〈0.05）,并导致细胞DNA断裂。DMF显著降低A549细胞内GSH水平（P〈0.05）,呈浓度依赖性。500μmol·L-1GSH预孵育1h,能有效阻断DMF诱导细胞内GSH耗竭,并减弱DMF触发细胞凋亡作用（P〈0.05）。结论细胞内GSH耗竭是DMF诱导人肺癌A549细胞凋亡作用机制之一。     

L-氨基酸氧化酶对人肺腺癌A549细胞增殖、凋亡的影响研究

目的:探讨L-氨基酸氧化酶(LAAO)对人肺腺癌A549细胞增殖、凋亡的影响,为临床上寻找新的肺癌治疗方法提供参考。方法:将A549细胞制成浓度为5×104个/mL的细胞悬液,根据LAAO干预浓度的不同,将其分为4组:2.41、4.82、9.64、19.28mg·mL-1干预组,各组均干预24、48、72h。镜下观察各组细胞形态学改变,采用MTT法检测细胞增殖抑制率,原位末端标记法检测细胞凋亡指数,另设立阴性对照组进行比较。结果:LAAO对A549细胞增殖的抑制率随时间延长和浓度增加而增加(P<0.05),凋亡指数随时间延长和浓度增加而增加(P<0.05)。结论:LAAO可抑制A549细胞增殖,诱导其凋亡,且呈时间、剂量依赖性。     

基于代谢组学的柠檬烯抗非小细胞肺癌作用机制研究

目的 采用非靶向代谢组学等方法，探究柠檬烯抑制非小细胞肺癌增殖的作用机制。方法 以肺癌A549细胞为研究对象，通过CCK-8法测定柠檬烯抑制A549细胞活力及IC₅₀；通过集落形成、流式细胞检测、铁含量测定及线粒体染色等实验，分别评价柠檬烯的体外抗肺癌及诱导铁死亡作用；代谢组学分析发现柠檬烯的潜在作用通路；最后采用Western blotting对相关通路主要蛋白进行验证。结果 与对照组相比，柠檬烯给药组可以显著抑制A549细胞的增殖及集落的形成，且呈剂量依赖性；光学显微镜观察发现，柠檬烯给药后A549细胞出现脱落现象，并可显著改变其形态；同时柠檬烯具有诱导A549细胞凋亡作用，并阻滞在G₀-G₁期；共聚焦显微镜发现柠檬烯作用后，A549细胞线粒体荧光减弱，同时细胞内铁含量亦显著增加，呈现典型的铁死亡表现；代谢组学研究发现谷胱甘肽(glutathione，GSH)代谢、精氨酸生物合成、D-谷氨酰胺和D-谷氨酸代谢及半胱氨酸和蛋氨酸代谢等多条差异代谢通路，这些通路与细胞内GSH合成密切相关；Western blotting实验发现，柠檬烯给药后细胞中SLC40A1、SLC7A11(xCT)及GPX4蛋白含量显著减少。结论 柠檬烯抗肺癌作用机制可能与降低肺癌细胞中GSH合成及增加Fe²⁺含量诱导其铁死亡有关。     

二氯乙酸钠联合顺铂诱导人肺腺癌A549细胞株凋亡的实验研究

目的研究二氯乙酸钠(Sodium dichloroacetate,DCA-Na)、顺铂(DDP)联合对人肺腺癌A549细胞株增殖和凋亡的影响及其作用机制。方法用MTT法检测DCA-Na、DDP应用对A549细胞增殖抑制作用的影响;流式细胞仪(Annexin V-FITC/PI法)检测DCA-Na、DDP单药及两药联合作用于A549细胞凋亡率的变化;用分光光度法检测DCA-Na作用于A549细胞后半胱氨酸天门冬氨酸蛋白酶(Caspase)-3、-8、-9蛋白的活性。结果DCA-Na、DDP单药组均对A549细胞增殖有抑制作用,且呈明显的剂量-时间依赖性。0.4、2μg/mL的DDP与37.5、75、150μg/mL的DCA-Na联合作用A549细胞24、48、72 h后的抑制率显著高于同浓度DDP单药组(P<0.05),且2μg/mL的DDP与75μg/mL的DCA联合在48 h表现为协同作用。流式细胞仪检测显示,A549细胞联合组凋亡率显著高于各单药组(P<0.05)。DCA-Na作用于A549细胞后,分别在12、24、48、72 h测得Caspase-3、-8、-9蛋白活性显著高于对照组(P<0.05)。结论 DCA-Na对人肺腺癌A549细胞的增殖有抑制作用,并且随着药物浓度增加、作用时间延长,其抑制作用也增加(呈剂量和时间依赖性)。一定浓度范围的DCA-Na和DDP联合作用于人肺腺癌A549细胞能够产生协同作用。DCA-Na可诱导人肺腺癌A549细胞凋亡,且与DDP联合后其诱导凋亡作用更为显著。     

Diclofenac potentiates the antitumor effect of cisplatin in a xenograft mouse model transplanted with cisplatin-resistant cells without enhancing cisplatin-induced nephrotoxicity

Cisplatin (CDDP) is a well-known anticancer agent, and CDDP–induced nephrotoxicity (CIN) is one of the most serious adverse effects. Previously, we revealed that while celecoxib reduces CIN, diclofenac does not appear to enhance it. Furthermore, we reported that diclofenac additively enhances the cytotoxic effect of CDDP on CDDP-resistant A549 cells (A549/DDP cells) and their spheroids. In addition, celecoxib reduces the cytotoxic effect of CDDP on A549/DDP cells while demonstrating an anticancer effect; however, it enhanced the effect of CDDP cytotoxicity on spheroids. Therefore, we evaluated the effects of diclofenac or celecoxib on CIN and the antitumor effect of CDDP in a xenograft mouse model transplanted with A549/DDP cells. Although CDDP did not decrease tumor size and tumor weight, these parameters were significantly reduced following co-administration with diclofenac when compared with the control group. Conversely, celecoxib marginally suppressed the antitumor effect of CDDP. Moreover, CDDP increased the mRNA levels of kidney injury molecule 1 (Kim-1), a renal disorder marker, in the kidneys of xenograft mice; treatment with celecoxib and diclofenac did not impact Kim-1 mRNA levels increased by CDDP. In conclusion, diclofenac potentiated the antitumor effect of CDDP without enhancing CIN.     

吉马酮对人肺癌A549细胞系增殖、凋亡的影响

目的研究吉马酮对人肺癌A549细胞增殖及凋亡的影响。方法用MTT比色法检测吉马酮对A549细胞增殖的抑制作用;采用流式细胞仪AnnexinV/PI双染法检测细胞凋亡率;采用电子显微镜观察吉马酮作用细胞后亚细胞结构的变化。结果吉马酮对人肺癌A549细胞的增殖有明显的抑制作用,并呈剂量效应关系;流式细胞仪结果显示,吉马酮可以诱导A549细胞凋亡,凋亡率与药物呈剂量效应关系;电子显微镜下经吉马酮处理后的细胞可见染色质浓聚、染色质边集等典型的凋亡改变,而空白对照组没有变化。结论吉马酮可以抑制肺癌A549细胞的增殖、诱导细胞凋亡。     

Impact of siRNA targeting pirh2 on proliferation and cell cycle control of the lung adenocarcinoma cell line A549

The aim of this study was to investigate the role of pirh2 (p53-induced RING-H2) protein in the proliferation, apoptosis and cell cycle control of the lung cancer cell line A549. Pirh2 expression was detected by immunofluorescence, Western blot analysis and real-time polymerase chain reaction (PCR). Cell proliferation was assessed by cell counting kit-8 (CCK-8). Cell cycle control and apoptosis were analyzed by flow cytometry. The results showed that pirh2 was expressed in the cytoplasm of A549 cells. The inhibition of pirh2 expression by siRNA (psiRNA-pirh2) resulted in reduced cell proliferation and increased apoptosis. In addition, the number of G₀/G₁ phase cells was increased but G₂/M cells were not affected significantly. Taken together, the inhibition of pirh2 expression in the lung adenocarcinoma cell line A549 resulted in reduced tumor cell growth via the inhibition of cell proliferation, the activation of apoptosis and the interruption of cell cycle transition.     

Survivin和Bcl-2调节槲皮素诱导的A549细胞凋亡

目的研究槲皮素诱导肺腺癌细胞A549凋亡,探讨survivin和Bcl-2在槲皮素诱导A549细胞凋亡中的调节作用。方法分别采用MTT法、荧光染色、流式细胞仪和免疫细胞化学观察了槲皮素对肺腺癌A549细胞增殖、凋亡、细胞周期和蛋白表达的影响。结果槲皮素抑制肺腺癌A549细胞增殖的作用明显,且呈浓度和时间依赖性。形态学检测显示出细胞凋亡的特征变化,槲皮素能使肺腺癌A549细胞周期阻滞于G0/G1期,且A549细胞survivin和Bcl-2蛋白表达同时下降,而caspase-3活性升高。结论槲皮素能诱导A549细胞凋亡,其机制可能是使肺腺癌A549细胞周期阻滞于G0/G1期,并同时下调survivin和Bcl-2蛋白的表达,直接激活caspase-3而诱导A549细胞凋亡。     

Trichostatin A sensitizes cisplatin-resistant A549 cells to apoptosis by up-regulating death-associated protein kinase

Aim:

To investigate the apoptosis-inducing effect of trichostatin A (TSA) in the human lung adenocarcinoma cisplatin-resistant cell line (A549/CDDP) and to examine whether TSA can enhance sensitivity to cisplatin treatment and the underlying molecular mechanisms of such an enhancement.

Methods:

Cell viability was evaluated using the Neutral Red assay. Apoptosis was assessed using Hoechst 33258 staining and flow cytometry analysis. Protein expression was detected by Western blotting. To determine the role of Death-associated protein kinase (DAPK) in TSA-induced apoptosis in the A549/CDDP cell line, cells were transfected with pcDNA3.1(+)-DAPK, which has a higher expression level of DAPK compared to endogenous expression, and DAPK activity was inhibited by both over-expression C-terminal fragment of DAPK which may competitive binding DAPK substrates to inhibit the function of DAPK and RNA interference.

Results:

TSA induced apoptosis in both A549 cells and A549/CDDP cells. TSA enhanced the sensitivity of A549/CDDP cells to cisplatin, along with concomitant DAPK up-regulation. When DAPK was over-expressed, A549/CDDP cells became sensitive to cisplatin and the cytotoxicity of TSA could be increased. Moreover, the cytotoxicity of TSA could be alleviated by inhibition of DAPK activity by the expression of a recombinant C-terminal fragment of DAPK or RNA interference.

Conclusion:

TSA induced sensitivity to cisplatin treatment in cisplatin-resistant A549 cells. The up-regulation of DAPK is one of the mechanisms mediating sensitization to TSA-induced apoptosis in cisplatin-resistant cells.     

姜黄素诱导人肺腺癌A549细胞脱落凋亡作用的研究

目的检测姜黄素诱导人肺腺癌细胞(A549)脱落凋亡的作用。方法采用DNA ladder法,流式细胞仪(FCM)技术结合PI及AnnexinV-FITC双标记染色试验方法及W estern-b lot法观察姜黄素是否能诱导A549脱落凋亡。结果A549细胞具有抗脱落凋亡的特性,而10μmol.L-1的姜黄素即可引起悬浮培养的A549细胞发生脱落凋亡。结论姜黄素可诱导人肺腺癌细胞(A549)脱落凋亡。     

雷公藤内酯醇对肺腺癌细胞系A549的体外抑制作用的研究

目的观察雷公藤内酯醇对肺腺癌细胞系A549体外生长特性的影响。方法分别采用MTT法、流式细胞仪、琼脂糖凝胶电泳以及荧光染色观察雷公藤内酯醇肺腺癌细胞系A549增殖、细胞周期以及凋亡的影响。结果14nmol.L-1～896nmol.L-1的雷公藤内酯醇均能抑制A549细胞的生长且生长抑制作用呈剂量以及时间依赖性。雷公藤内酯醇在低浓度(14nmol.L-1)条件下,能诱导A549细胞发生细胞周期阻滞,阻滞部位在S期;高浓度(55,112mol.L-1)的雷公藤内酯醇使A549阻滞在G2/M期,并诱导其发生凋亡。结论雷公藤内酯醇能抑制A549细胞的生长,使其阻滞在S期和G2/M期,并诱导其发生凋亡。     

AZIN-1小分子抑制剂抗非小细胞肺癌活性研究

目的研究鸟氨酸脱羧酶抗酶抑制因子-1(AZIN-1)小分子抑制剂对非小细胞肺癌的抑制作用及机制。方法通过CCK-8法检测A549细胞增殖;流式细胞术(Annexin V-FITC/PI双染)分析A549细胞凋亡;蛋白质免疫印迹实验检测A549细胞内鸟氨酸脱羧酶(ODC)、鸟氨酸脱羧酶抗酶-1(AZ-1)和AZIN-1的表达;流式细胞术(PI单染)分析A549细胞周期;高效液相色谱法检测A549细胞内总多胺含量。结果AZIN-1小分子抑制剂能够显著抑制A549细胞的增殖,使细胞发生G0/G1周期阻滞,并诱导A549细胞发生凋亡,显著抑制AZIN-1和ODC的表达,干扰细胞内多胺代谢,降低细胞内总多胺含量。结论AZIN-1小分子抑制剂对A549细胞具有显著的生长抑制作用,其作用机制可能与诱导细胞凋亡和干扰多胺代谢有关。     

慢病毒介导CK18基因沉默对人乳腺癌BT549细胞增殖、凋亡和侵袭能力的影响

摘要：目的 检测靶向沉默细胞角蛋白18（CK18）基因对人乳腺癌BT549细胞增殖、凋亡、侵袭运动的影响,并探 讨其潜在的分子机制。方法 建立 CK18 稳定沉默的 BT549 细胞株,分为 3 组,以 CK18（CK18-sh21、CK18-sh22、 CK18-sh23及CK18-sh24）靶向沉默的细胞为实验组CK18-shRNA,加入空载体的为阴性对照（sh-Con）组,未处理为 空白对照（Wt）组。采用蛋白印迹法（Western blot）对细胞系进行CK18表达鉴定。采用CCK-8法、平板克隆形成法检 测 CK18 表达缺失对细胞增殖能力的影响;通过流式细胞技术（PE–Annexin V 双染法）检测 CK18 基因沉默后对 BT549细胞凋亡的影响;通过PI-FACS 法检测沉默CK18对BT549细胞周期的影响;采用划痕试验、Transwell法检测 CK18沉默对细胞运动及侵袭能力的影响;采用Western blot检测与侵袭转移相关的分子E-钙黏蛋白（E-cadherin）和 波形蛋白（vimentin）表达情况。结果 建立了CK18沉默的BT549细胞系,CK18的表达被显著抑制,CK18-sh23组相 对sh-Con组抑制率最高,可达73%。与Wt组、sh-Con组相比,CK18-shRNA细胞增殖能力在24 h、48 h和72 h降低, 克隆形成能力下降,细胞运动、侵袭能力下降,细胞凋亡率和G2期细胞比例均增加（P＜0.05）。与sh-Con组和Wt组 比较,CK18表达降低能促进E-cadherin表达,抑制vimentin表达（P＜0.05）。结论 CK18基因沉默能有效抑制人乳 腺癌BT549细胞的增殖、运动、侵袭,诱导细胞的凋亡,并阻滞细胞周期;CK18还可能通过诱导EMT发生参与乳腺癌 BT549细胞的侵袭转移过程。     

Diterpenoid C of Radix Curcumae: An inhibitor of proliferation and inducer of apoptosis in human colon adenocarcinoma cells acting via inhibiting MAPK signaling pathway

Context: Radix Curcumae is a traditional Chinese medicine that possesses antitumor properties, from which a new compound, diterpenoid C, was previously isolated and characterized.

Objective: In this study, using human colon adenocarcinoma SW620 cells, we further investigated the antitumor effects of diterpenoid C and the underlying mechanisms.

Materials and methods: Cell proliferation was assessed with the MTT assay. Cell apoptosis and cell-cycle progression were analyzed with flow cytometry. The expression of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (p38 MAPK), and their phosphorylated forms, as well as caspase-3 protein levels were examined with Western blots.

Results: Diterpenoid C could inhibit the proliferation of SW620 cells in a dose- and time-dependent manner. The median inhibitory concentration (IC₅₀) at 24, 48, and 72?h were 28.31, 15.58, and 6.14?μg/ml, respectively. The inhibition of proliferation was found to be statistically significant as compared with the well-established drugs 5-fluorouracil (5-Fu) and oxaliplatin (L-OHP) (p?Discussion and conclusion: Diterpenoid C inhibits proliferation and induces apoptosis of cancer cells by suppressing the MAPK signaling pathway and inducing apoptotic factor caspase-3. Our results suggest that this novel compound might become a potent chemotherapeutic agent for the treatment of colon cancer and further studies are warranted.     

Propyl gallate decreases the proliferation of Calu-6 and A549 lung cancer cells via affecting reactive oxygen species and glutathione levels

Propyl gallate (3,4,5-trihydroxybenzoic acid propyl ester, PG) has an anti-proliferative effect in various cells. In this study, Calu-6 and A549 lung cancer cells were used to examine the anti-proliferative effect of PG in relation to reactive oxygen species (ROS) and glutathione (GSH) levels. PG (100–1,600 μM) dose-dependently inhibited the proliferation of Calu-6 and A549 cells at 24 h, and PG at 800–1,600 μM strongly induced cell death in both cell lines. PG (800–1,600 μM) increased cellular metabolism in Calu-6 but not A549 cells at 4 h. PG either increased or decreased ROS levels, including O₂˙⁻ and ˙OH, depending on the incubation doses and times of 1 or 24 h. Even these effects differed between Calu-6 and A549 cell types. PG reduced the activity of superoxide dismutase (SOD) in Calu-6 cells, and it augmented the activity of catalase in A549 cells. PG dose-dependently increased the number of GSH depleted cells in both Calu-6 and A549 cells at 24 h. In addition, PG decreased GSH levels in both lung cancer cells at 1 h. Furthermore, diethyldithiocarbamate (DDC; an inhibitor of SOD) and 3-amino-1,2,4-triazole (AT; an inhibitor of catalase) differently affected cellular metabolism, ROS and GSH levels in PG-treated and PG-untreated Calu-6 and A549 cells at 1 h. In conclusion, PG dose-dependently decreased the proliferation of Calu-6 and A549 lung cancer cells, which was related to changes in ROS levels and the depletion of GSH.     

老年患者胃癌组织的体外化疗药敏性与凋亡抑制蛋白p53、生存素、Bcl-2表达的关系

目的探讨老年患者胃癌肿瘤组织的体外化疗药物敏感性与凋亡抑制蛋白表达的关系。方法 MTT法检测65例老年胃癌患者(≥65岁)及58例对照组患者(<65岁)肿瘤细胞原代培养药物敏感性。应用免疫组化法检测肿瘤组织凋亡抑制蛋白p53、生存素和Bcl-2的表达。结果10种化疗药物中,氟尿嘧啶(5-FU)、长春新碱(VCR)、奥沙利铂(L-OHP)、表阿霉素(eADM)、丝裂霉素(MMC)对老年患者肿瘤细胞的抑制率低于对照组(P<0.05)。老年组生存素、Bcl-2表达高于对照组(P<0.01),且两者表达存在正相关性(P<0.05);对照组p53的表达与Bcl-2存在正相关(P<0.01)。老年胃癌患者p53的表达与紫杉醇(PTX)、顺铂(CDDP)对肿瘤细胞的抑制率呈负相关(P<0.01),生存素与5-FU、PTX、L-OHP、CDDP、eADM的抑制率呈负相关(P<0.05),Bcl-2表达则与VCR、足叶乙甙(VP-16)、羟基喜树碱(HCPT)、PTX、吡喃阿霉素(THP)呈负相关(P<0.05);对照组p53与CDDP的抑制率呈负相关(P<0.05),生存素表达则与5-FU、VCR、HCPT呈负相(P<0.01),Bcl-2表达与VP-16、CDDP对肿瘤细胞的抑制率呈负相关(P<0.05),但与L-OHP的抑制率正相关(P<0.05)。结论老年胃癌患者与对照组存在不同的多药耐药表型,凋亡抑制蛋白在老年胃癌多药耐药中起重要作用。     

黄芩苷对香烟烟雾提取物诱导的细胞损伤保护作用研究

目的研究黄芩苷对香烟烟雾提取物（cigarette smoke extract,CSE）诱导的人肺泡上皮细胞损伤的影响,并初步探讨其机制。方法制备CSE,用不同浓度黄芩苷对人肺泡上皮细胞A549进行预处理,再用CSE刺激细胞。用MTT法检测细胞存活率,流式细胞术测定细胞凋亡率,彗星实验观察DNA损伤情况,荧光法测定细胞内活性氧（reactive oxygen species,ROS）含量。结果随着CSE浓度的增加和作用时间的延长,细胞存活率下降,各组之间有统计学差异（P〈0.05）;黄芩苷能减少CSE诱导的细胞存活率下降,抑制CSE诱导的细胞内ROS的产生,并有剂量依赖关系（P〈0.05或P〈0.01）;黄芩苷＋CSE组细胞的彗星尾长、尾部DNA含量、尾距、Olive尾距均小于CSE组（P〈0.05）,并且黄芩苷可以减少CSE导致的细胞凋亡。结论黄芩苷可以拮抗CSE对细胞的损伤,提高细胞的存活率,降低凋亡率,其原因可能与黄芩苷能降低细胞ROS含量,减少DNA损伤有关。     

MAP30-PEG结合物对A549体外细胞增殖作用的研究

目的探讨苦瓜籽核糖体失活蛋白MAP30及其聚乙二醇修饰物对人肺腺癌细胞A549增殖、细胞凋亡的影响和caspase3相关凋亡途径的诱导作用。方法用MTT法测定MAP30和MAP30-PEG结合物对人肺腺癌细胞A549的抑制率;通过Hoechst33258荧光染色观察A549细胞凋亡形态,并用流式细胞术测定细胞凋亡率以及用western blot检测凋亡细胞caspase3表达。结果 MAP30和MAP30-PEG结合物均对A549有抑制作用,且呈时间和剂量依赖性关系;MAP30-PEG结合物对A549细胞增值抑制率约为MAP30的60%;Hoechst33258荧光染色后均呈典型凋亡形态;流式细胞术检测显示,MAP30和MAP30-PEG结合物作用于A549细胞48 h后均可使A549细胞呈现Sub-G1凋亡峰,凋亡率分别为58.7%、42.7%;MAP30和MAP30-PEG结合物对胞内caspase3在凋亡过程中显示有激活作用。结论 MAP30和MAP30-PEG结合物均对A549增殖有明显的抑制作用;两者均能通过caspase3途径诱导细胞凋亡。