VX-680抑制肝癌HepG2细胞恶性表型的分子机制研究

目的探究VX-680对肝癌HepG2细胞恶性表型的影响及其分子机制。方法取肝癌细胞系HepG2细胞进行培养,分别给予0μmol/L、4μmol/L、8μmol/L、16μmol/L浓度VX-680进行处理,采用四甲基偶氮唑盐微量酶反应比色(MTT)法、平板克隆法、4',6-二脒基-2-苯基吲哚(DAPI)法、体外HUVEC小管形成实验检测肝癌HepG2细胞增殖、凋亡及血管生成等生物学行为,分别采用逆转录聚合酶链式反应(RT-PCR)、Western Blot法测定细胞磷脂酰肌醇3-激酶(PI3K)、丝氨酸苏氨酸激酶(Akt)、血管内皮生长因子(VEGF)基因mRNA、蛋白表达情况。结果①VX-680各浓度处理组细胞增殖抑制率显著高于对照组(P<0.05),克隆形成数显著低于对照组(P<0.05),随着浓度的升高,增殖抑制率、克隆形成数升高或降低幅度加大(P<0.05)。②DAPI染色实验示,各浓度VX-680作用下细胞可见不同程度凋亡,随浓度升高细胞凋亡数增多,组间比较差异具统计学意义(P<0.05)。③小管生成实验结果显示,与0μmol/L VX-680组比较,4μmol/L、8μmol/L、16μmol/L浓度VX-680作用下小管形成数逐渐减少,随着浓度的升高,小管生成数减少,差异具统计学意义(P<0.05)。④RT-PCR、Western-blot实验显示,随着处理浓度的升高,细胞PI3K、Akt、VEGF基因mRNA、蛋白表达均显著降低,差异具统计学意义(P<0.05)。结论VX-680可抑制肝癌HepG2细胞增殖、凋亡及血管生成作用,且存在明显的剂量效应,这一作用机制可能与其抑制PI3K/Akt通路的活性及VEGF的表达相关。     

胡椒碱对人肝癌HepG2细胞抗肿瘤活性的体外实验研究

目的 探讨胡椒碱(piperine)对人HpeG2肝癌细胞株的增殖、杀伤和细胞凋亡的影响,为肝癌的治疗提供理论依据.方法 体外培养的HpeG2细胞,采用MTT比色法检测不同浓度胡椒碱对体外培养的HepG2细胞和新分离的外周血白细胞的增殖抑制作用.Hoechst 33258染色观察细胞凋亡形态,采用流式细胞术测定胡椒碱对HepG2细胞的凋亡.结果 胡椒碱对HepG2细胞增殖的抑制率随着浓度的升高而增加,半量抑制浓度(IC50)为15.13±3.21 μmol/L,低于其对外周血白细胞的抑制率(64.52±5.32 μmol/L).Hoechst 33258染色后,胡椒碱处理癌细胞组表现出典型的细胞凋亡特征,流式细胞仪检测20 μmol/L的胡椒碱处理HepG2细胞24 h后,细胞凋亡率由对照组的2.89%上升到了21.76%.结论 胡椒碱具有抑制HepG2细胞增殖和诱导凋亡的抗肿瘤活性,有应用于肝癌治疗的潜在价值.     

mTOR信号通路调控1,25二羟维生素D_3抑制喉癌细胞Hep-2细胞增殖的研究

目的研究1,25二羟维生素D3抑制喉癌细胞Hep-2细胞增殖作用以及对雷帕霉素靶蛋白(mTOR)信号通路的影响。方法用不同剂量1,25二羟维生素D3(10-8 mol/L、10-7 mol/L、10-6 mol/L)分别处理Hep-2细胞24、48、72h,四甲基偶氮唑蓝法(MTT)检测Hep-2细胞的增殖情况,并计算抑制率;采用流式细胞仪分析1,25二羟维生素D3对Hep-2细胞周期分布的影响,Western blot检测1,25二羟维生素D3对mTOR信号通路的影响。结果不同浓度1,25二羟维生素D3均可抑制Hep-2细胞增殖,改变细胞周期分布,使G0/G1期Hep-2细胞比例增高。1,25二羟维生素D3干预后Hep-2细胞TSC1、TSC2蛋白表达较对照组增高(P0.01),Rheb蛋白表达明显降低;mTOR蛋白及其磷酸化水平表达与对照组比较均降低(P0.01),mTOR蛋白磷酸化表达降低尤为明显(P0.01);4EBP-1蛋白表达较对照组增高(P0.01)。结论 1,25二羟维生素D3改变喉癌细胞Hep-2细胞周期分布,影响mTOR信号通路蛋白表达,从而抑制细胞增殖。     

STAT3反义寡核苷酸对HepG2肝癌细胞增殖抑制和凋亡诱导作用

目的:探讨STAT3反义寡核苷酸(ASODN)对HepG2细胞增殖的抑制作用和细胞凋亡的诱导作用。方法:HepG2细胞体外培养,人工合成并硫代修饰STAT3 ASODN,通过脂质体转染进入HepG2细胞,倒置显微镜下观察细胞形态学变化,MTT法检测细胞增殖抑制程度,原位末端标记法检测细胞凋亡指数,RT-PCR检测细胞中STAT3 mRNA的表达水平。结果:STAT3 ASODN各浓度组对HepG2细胞的增殖有明显的抑制作用,能明显诱导细胞凋亡。结论:STAT3 ASODN能够诱导HepG2细胞凋亡。     

2-甲氧基雌二醇诱导K562细胞凋亡及机制研究

本研究探讨2-甲氧基雌二醇（2-ME2）对K562细胞的诱导凋亡作用及其机制。采用不同浓度2-ME2处理K562细胞,MTT法检测K562细胞的增殖活性,DNA琼脂糖凝胶电泳和Annexinv／PI双染色法检测K562细胞的凋亡效应,流式细胞术检测细胞线粒体膜电位的变化,RT-PCR和Western blot方法分别检测相关基因mRNA和／或蛋白的表达变化。结果表明：2-ME2抑制K562细胞增殖呈时间和剂量依赖性;48小时的半数抑制浓度（IC。）为2μmol／L;2μmol／L2-ME2作用于K562细胞24、48、72小时,DNA凝胶电泳分析可见典型DNA梯形条带;Annexinv／PI双染色法检测显示,细胞凋亡率分别为13．78％、22．32％和29．43％,而对照组凋亡率仅为1．78％（P〈0．05）;1、2和4μmol／L2-ME2分别处理K562细胞24小时,流式细胞术检测显示细胞线粒体膜电位下降;2μmol／L2-ME2处理K562细胞24、48和72小时,K562细胞中bcr／abl、bcl-2mRNA表达下调,而baxmRNA表达上调,Bcl-2、procaspase-3、procaspase-9、PARP（116 kD）和p-Akt蛋白表达下调,胞浆Cyto-C和PARP活性片段（85kD）表达上调,而对总Akt蛋白表达无影响。结论：2-ME2通过升高bax／bcl-2比值降低线粒体膜电位、促使细胞色素C（Cyto-c）释放入胞浆、触发K562细胞的线粒体凋亡途径,活化caspase-3,导致K562细胞凋亡并抑制其增殖;通过下调bcr／ab1 mRNA表达以阻断P13K／Akt信号通路也参与了该过程。     

新型bcl-2反义寡核苷酸F951提高白血病细胞对阿糖胞苷的敏感性

为了研究新型bcl-2反义寡核苷酸F951提高白血病细胞对化疗药物的敏感性，用不同浓度的F951及F951联合小剂量Ara—C与HL-60细胞共培养后，采用台盼蓝拒染法、MTT比色法检测HL-60细胞增殖；用流式细胞术和RT-PCR法检测Bcl-2蛋白及其mRNA表达；以DNA片段化分析和TdT酶介导的缺口末端标记(TUNEL)法检测凋亡细胞。结果表明，F951与Ara—C联用组细胞生长抑制率最高，药物处理96小时后，台盼蓝拒染率明显低于单纯Ara—C处理组；MTT检测A值与未处理组相比，FNS对照组、Ara—C组、F951组、F951 Ara—C组细胞抑制率分别为：2墙％、27．63％、37．66％、57．24％，F951处理后HL-60细胞Bcl-2mRNA水平下降，Bcl-2蛋白减少，凝胶电泳可见典型的梯形带，F951与Ara—C联用后，诱导DNAladder的作用更加明显，凋亡细胞多见．结论：F951可下调bcl-2基因表达，促进细胞凋亡而增强Ara—C的抗肿瘤作用。     

Mesenchymal stem cells protect from acute liver injury by attenuating hepatotoxicity of liver natural killer T cells in an inducible nitric oxide synthase‐ and indoleamine 2,3‐dioxygenase‐dependent manner

The effects of mesenchymal stem cells (MSCs) on the phenotype and function of natural killer T (NKT) cells is not understood. We used concanavalin A (Con A) and α‐galactosylceramide (α‐GalCer)‐induced liver injury to evaluate the effects of MSCs on NKT‐dependent hepatotoxicity. Mouse MSCs (mMSCs) significantly reduced Con A‐ and α‐GalCer‐mediated hepatitis in C57Bl/6 mice, as demonstrated by histopathological and biochemical analysis, attenuated the influx of inflammatory [T‐bet⁺, tumour necrosis factor‐α (TNF‐α), interferon‐γ (IFN‐γ)‐producing and GATA3⁺, interleukin‐4 (IL‐4)‐producing] liver NKT cells and downregulated TNF‐α, IFN‐γ and IL‐4 levels in the sera. The liver NKT cells cultured in vitro with mMSCs produced lower amounts of inflammatory cytokines (TNF‐α, IFN‐γ, IL‐4) and higher amounts of immunosuppressive IL‐10 upon α‐GalCer stimulation. mMSC treatment attenuated expression of apoptosis‐inducing ligands on liver NKT cells and suppressed the expression of pro‐apoptotic genes in the livers of α‐GalCer‐treated mice. mMSCs reduced the cytotoxicity of liver NKT cells against hepatocytes in vitro. The presence of 1‐methyl‐dl ‐tryptophan, a specific inhibitor of indoleamine 2,3‐dioxygenase (IDO), or l ‐N^G‐monomethyl arginine citrate, a specific inhibitor of inducible nitric oxide synthase (iNOS), in mMSC‐conditioned medium injected into α‐GalCer‐treated mice, counteracted the hepatoprotective effect of mMSCs in vivo and restored pro‐inflammatory cytokine production and cytotoxicity of NKT cells in vitro. Human MSCs attenuated the production of inflammatory cytokines in α‐GalCer‐stimulated human peripheral blood mononuclear cells in an iNOS‐ and IDO‐dependent manner and reduced their cytotoxicity against HepG2 cells. In conclusion, MSCs protect from acute liver injury by attenuating the cytotoxicity and capacity of liver NKT cells to produce inflammatory cytokines in an iNOS‐ and IDO‐dependent manner.     

阻断血管内皮生长因子与表皮生长因子受体协同信号影响HepG2肝癌细胞生长的实验研究

目的探讨阻断血管内皮生长因子（VEGF）与表皮生长因子受体（EGFR）协同信号对HepG2肝癌细胞生长的影响。方法体外培养HepG2肝癌细胞株,分别将含不同浓度（10-2、10-3、10-4、10-5μg/μL）抗VEGF抗体与抗EGFR抗体的培养液与HepG2肝癌细胞共同培养12、24、4-8h,采用四甲基偶氮唑盐微量酶反应比色法（MTT）比色法计算细胞生长抑制率。以抗体的不同浓度对HepG2肝癌细胞抑制率作图,得到剂量反应曲线。结果抗VEGF抗体和抗EGFR抗体对HepG2肝癌细胞生长的抑制均呈浓度依赖性,并且有一定的量效关系。结论阻断VEGF与EGFR协同信号可抑制HepG2抗体肝癌细胞的增殖,具有剂量依赖性,可诱导细胞凋亡。     

Cytotoxicity of abnormal Savda Munziq aqueous extract in human hepatoma (HepG2) cells

Abnormal Savda Munziq (ASMq) is a traditional Uighur medicinal herbal preparation commonly used to treat diseases such as diabetes, cardiovascular diseases, chronic asthma and especially digestive cancer. Earlier studies have shown that ASMq is a free radical scavenger and could prevent mitochondrial and DNA oxidative damage. In this study, we tested the effects of aqueous extract of ASMq on human hepatoma cells (HepG2) to explore the possible mechanism of its putative anticancer properties. Aqueous extract of ASMq was tested on HepG2 proliferation (MTT assay) at 72 h, cell viability at 48 h (neutral red assay), lactate dehydrogenase release over 48 or 72 h as a measure of cytoplasmic leakage, lipid peroxidation (malondialdehyde-thiobarbituric acid adducts) at 48 h, and incorporation of [3H]-leucine, [3H]-thymidine and [3H]-uridine into cellular protein, DNA and RNA, respectively, at 24 or 48 h to assess the inhibition effects to cellular macromolecule synthesis. Our results showed a significant (P < 0.05) time- and concentration-dependent inhibition of HepG2 proliferation and viability, with increased cytoplasmic leakage, and time- and concentration-dependent inhibition of protein, DNA and RNA synthesis. No lipid peroxidation was found at these concentrations. The results of the present study suggest that the putative anticancer mechanisms of ASMq may at least involve cytotoxicity.     

Sporamin induce apoptosis in human tongue carcinoma cells by down‐regulating Akt/GSK‐3 signaling

We investigated the effects of sporamin, the major soluble protein with a kunitz‐type trypsin inhibitory activity in the root tuber of the sweet potato, on cell proliferation, apoptosis, Akt/GSK‐3 signaling and its related genes to provide more insights in the mechanism behind the inhibitory effects of sporamin in a human tongue cancer line Tca8113. In this study, sporamin inhibited cell proliferation and induced apoptosis in Tca8113 cells in a concentration‐dependent and time‐dependent manner. Consistently, Bax was up‐regulated and Bcl‐2 was down‐regulated in sporamin‐treated cells. Furthermore, Akt/GSK‐3 signaling was down‐regulated in sporamin‐treated cells. Consistently, the phosphorylated Bad was significantly declined in sporamin‐treated Tca8113 cells. These results suggest the antiproliferative effects of sporamin in Tca8113 cells might result partly from induction of apoptosis by down‐regulating Akt/GSK‐3 pathway.     

2-甲氧基雌二醇上调Bax/BCL-2比例诱导淋巴瘤Raji细胞凋亡的研究

目的:研究2-甲氧基雌二醇(2-ME2)对淋巴瘤Raji细胞的作用及其作用机制。方法:用不同浓度2-ME2作用于淋巴瘤Raji细胞,CCK8法检测2-ME2对Raji细胞增殖的影响;流式细胞仪FITC/PI双标法检测细胞早期的凋亡;蛋白印迹法检测2-ME2对Raji细胞BCL-2、Bax、Caspase-3、C-myc蛋白表达的影响。结果:2-ME2对Raji细胞的增殖具有明显抑制作用,其抑制率随着药物浓度的增高而增加,随着药物作用时间的延长而显著增高(r=0.9215)。流式细胞仪FITC/PI双染色法结果显示,2.5μmol/L 2-ME2处理24 h组的细胞凋亡率为(33.79±1.63)%,而48 h组的凋亡率高达(51.90±2.72)%,对照组Raji细胞为(7.08±0.36)%。2.5μmol/L 2-ME2处理Raji细胞12 h后,蛋白印迹检测结果显示,Bax蛋白表达上调,BCL-2蛋白下调,而Caspase-3蛋白表达亦上调,C-myc蛋白表达下调,之间均具有时效性关系。结论:2-ME2对淋巴瘤Raji细胞具有明显的抑制作用,且呈剂量和时间依赖性。其对淋巴瘤Raji细胞的作用机制可能与上调Bax/BCL-2比例,激活Caspase-3诱导癌细胞凋亡有关,下调C-myc蛋白表达也参与了凋亡过程。     

EGF诱导肝癌细胞系HepG2增殖及其作用机制

目的观察表皮生长因子（EGF）对肝癌细胞系HepG2增殖的影响,初步探讨C-erbB2在其中的作用机制。方法以不同浓度（0、0.1、1、10、100μg.L-1）EGF作用于肝癌细胞系HepG2,采用MTT法观察EGF对HepG2增殖的影响;采用RT-PCR检测C-erbB2 mRNA的表达变化。结果 EGF能呈剂量依赖方式诱导肝癌细胞系HepG2的增殖;10μg.L-1EGF可显著增强肝癌细胞系HepG2 C-erbB2 mRNA的表达。结论 EGF可诱导肝癌细胞株HepG2的增殖,其机制可能与上调原癌基因C-erbB2的表达有关。     

Allyl‐isatin suppresses cell viability,induces cell cycle arrest,and promotes cell apoptosis in hepatocellular carcinoma HepG2 cells

The anticancer effect of the newly synthesized isatin derivative, N‐allyl‐isatin (Allyl‐I), was evaluated in vitro with human hepatocellular carcinoma HepG2 cells. Cell viability was detected by cell counting kit‐8 (CCK8) assay. Acridine orange (AO)/ethidium bromide (EB) double staining was used to observe the cell morphology. Flow cytometry was used to assess the effects of Allyl‐I on the cell cycle, apoptosis rate, and mitochondrial membrane potential (MMP). Western blot analysis was performed to detect the influence of Ally1‐I on the expression of cytochrome c (cyt c), Bax, Bcl‐2, and cleaved caspase‐3. Allyl‐I significantly inhibited HepG2 cell viability in a time‐ and dose‐dependent manner. Allyl‐I can induce cell cycle arrest in HepG2 cells at the G2/M phase. Apoptotic nuclear morphological changes were observed after AO/EB double staining. Fluorescein isothiocyanate‐conjugated Annexin V (Annexin V‐FITC) and propidium iodide (PI) double staining showed that the apoptotic rates significantly increased in the presence of Allyl‐I. Rhodamine 123 staining indicated that Allyl‐I can decrease the MMP. Allyl‐I also altered the expression of mitochondrial apoptosis‐related proteins. Protein levels of cyt c and cleaved caspase‐3 were upregulated following Allyl‐I treatment. By contrast, the Bcl‐2/Bax ratio decreased. Results suggest that Allyl‐I suppresses cell viability, induces cell cycle arrest, and promotes cell apoptosis in HepG2 cells. Furthermore, the induction of apoptosis might be correlated with the mitochondrial pathway.     

Thiazolidenediones induce tumour-cell apoptosis through the Akt-GSK3β pathway

What is known and Objective: Prostate cancer is a major health threat for men. Thiazolidenediones (TZDs) are synthetic ligands of the peroxisome proliferator‐activated receptor γ (PPARγ), and previous studies have shown that TZDs induce apoptosis of prostate cancer cells independently of PPARγ activation. However, the exact mechanism of these effects remains unknown. Our objective was to investigate the effects of TZDs on apoptosis and on the serine/threonine kinase pathway, Akt, and glycogen synthase kinase 3β (GSK3β). Methods: LNCaP cells, a type of prostate cancer cells (derived from left supraclavicular lymph node of human prostrate carcinoma), were cultured in DMEM medium, and cell viability was evaluated with a colorimetric assay using MTT level. The total and phosphorylated protein level of Akt and GSK3β were detected by Western blotting. Results and Discussion: The apoptosis‐inducing effect of TZDs on prostate cancer cells involves the inhibition of Akt phosphorylation. Furthermore, TZDs induce inactivation of GSK3β, a multifunctional kinase that mediates essential events promoting prostate cancer development and acquisition of androgen independence. In addition, the GSK3β inhibitor lithium chloride sensitizes prostate cancer cells to TZDs cytotoxicity. What is new and Conclusion: Our data suggest that modulation of Akt‐GSK3β pathway is involved in the cell death pathway engaged by TZDs in prostate cancer cells. This reveals another possible mechanism of TZDs on apoptosis in prostate cancer. Inhibition of the Akt‐GSK3β cascade may be a useful approach in prostate cancer.     

塞来昔布联合索拉非尼对人肝癌HepG2细胞迁移与侵袭能力的影响

目的评价塞来昔布联合索拉非尼对人肝癌HepG2细胞迁移与侵袭能力的影响。方法采用MTT法检测药物对HepG2细胞增殖的抑制率;通过划痕实验、Transwell实验评价药物对HepG2细胞迁移与侵袭作用的影响;采用Western blot法检测相关蛋白E-cadherin、COX-2、Notch1、Snail的表达。结果塞来昔布与索拉非尼联用有协同抑制HepG2细胞增殖的作用。与对照组比较,两药单独用药及联合用药均可抑制HepG2细胞迁移与侵袭作用(P<0.05或P<0.01)。塞来昔布无显著增强索拉非尼诱导HepG2细胞E-cadherin表达增加的作用,也无显著降低索拉非尼诱导HepG2细胞Notch1、Snail表达下降的作用;索拉非尼无显著增强塞来昔布诱导HepG2细胞COX-2表达下降的作用。结论塞来昔布可增强索拉非尼的抗HepG2细胞增殖作用,但不影响索拉非尼抑制的HepG2细胞迁移与侵袭作用。     

曲列格酮对Hep G2肝癌细胞增殖、COX-2表达和前列腺素E2水平的影响

目的　探讨曲列格酮 (TGZ)对HepG2肝癌细胞增殖的影响。方法　TGZ处理HepG2细胞后 ,用MTT、[3 H]-胸苷摄入、Northern杂交、RT -PCR、Western印迹等方法分别测定细胞增殖、COX - 2表达及PGE2水平。结果　TGZ以剂量依赖方式抑制细胞增殖 ,并下凋COX - 2表达及抑制PGE2产生。结论　TGZ抑制HepG2肝癌细胞增殖 ,这种抑制作用可能与COX - 2表达减少有关。     

Preconditioning with interleukin‐1 beta and interferon‐gamma enhances the efficacy of human umbilical cord blood‐derived mesenchymal stem cells‐based therapy via enhancing prostaglandin E2 secretion and indoleamine 2,3‐dioxygenase activity in dextran sulfate sodium‐induced colitis

Preconditioning with inflammatory cytokines has improved mesenchymal stem cells characteristics, including differentiation and immunomodulating functions. In this study, we developed a preconditioning combination strategy using interleukin‐1beta (IL‐1β) and interferon‐gamma (IFN‐γ) to enhance the immuneregulatory ability of human umbilical cord blood‐derived mesenchymal stem cells (hUCB‐MSCs). Our results showed that hUCB‐MSCs preconditioned with IL‐1β and IFN‐γ (primed hUCB‐MSCs) created a statistically significant decrease in peripheral blood mononuclear cell proliferation, indicating that their immunosuppressive ability was increased. The secretion of PGE2, cyclooxygenase 2 mRNA expression, and indoleamine 2,3‐dioxygenase (IDO) mRNA expression in primed hUCB‐MSCs was significantly higher than those in the untreated hUCB‐MSCs or the IL‐1β or IFN‐γ only treated hUCB‐MSCs. When inhibitors of IDO and PGE2 were treated, peripheral blood mononuclear cell proliferation, which is inhibited by primed hUCB‐MSCs, was recovered. We found that Th1 T cell differentiation was also inhibited by PGE2 and IDO in the primed hUCB‐MSCs, and Tregs differentiation was increased by PGE2 and IDO in the primed hUCB‐MSCs. Furthermore, the primed hUCB‐MSCs as well as supernatants increase CD4⁺ T cells migration. We demonstrated the therapeutic effects of primed hUCB‐MSCs in dextran sulfate sodium‐induced colitis model. In conclusion, we have demonstrated that primed hUCB‐MSCs simultaneously enhance PGE2 and IDO and greatly improve the immunoregulatory capacity of MSCs, and we have developed an optimal condition for pretreatment of MSCs for the treatment of immune diseases. Our results raise the possibility that the combination of PGE2 and IDO could be therapeutic mediators for controlling immunosuppression of MSCs.     

FH535抑制人肝癌细胞HepG2增殖及cyclin D表达

目的 探讨β-catenin抑制剂FH535对人肝癌细胞系HepG2增殖的影响及可能机制.方法 HepG2细胞分为对照组和FH535用药组,使用改良3-(4,5-二甲基噻唑-2)-2,5-二苯基四氮唑溴盐比色法(MTS)检测FH535对HepG2细胞增殖的影响,以Western blot法检测HepG2细胞β-catenin以及cyclin D蛋白表达水平,用实时荧光定量聚合酶链式反应(PCR)检测HepG2细胞cyclin D mRNA水平.结果 FH535能够显著抑制HepG2细胞的增殖,呈时间和剂量依赖性.与对照组相比,FH535给药组HepG2细胞内β-catenin蛋白表达无差异.FH535给药组细胞wnt/β-catenin信号通路的靶基因cyclin D的mRNA和蛋白的表达显著下降,与对照组相比差异有统计学意义(P<0.0001).结论 FH535通过抑制cyclin D mRNA及cyclin D蛋白表达而抑制HepG2细胞增殖.     

康莱特对HepG2细胞凋亡及其Caspase-3和Survivin表达影响

目的观察康莱特注射液对HepG2肝癌细胞凋亡及半胱氨酸天冬氨酸蛋白酶-3（Caspase-3）和存活素（Survivin）表达的影响,并初步探讨其作用机制。方法分别采用体积分数0.005、0.010、0.015、0.020的康莱特体外培养HepG2细胞。采用MTT法检测HepG2细胞抑制率,流式细胞仪检测HepG2凋亡情况以及Caspase-3和Survivin表达的变化。结果康莱特能明显抑制HepG2肝癌细胞生长,且呈时间和浓度依赖性。康莱特组中Caspase-3、Survivin蛋白的表达与对照组比较,差异有显著性（P〈0.01）。结论康莱特可抑制HepG2肝癌细胞增殖,并可通过提高Caspase-3蛋白表达和降低Survivin蛋白表达诱导HepG2肝癌细胞凋亡。