Heme Oxygenase-1 Induced by Aprotinin Inhibits Vascular Smooth Muscle Cell Proliferation Through Cell Cycle Arrest in Hypertensive Rats

Spontaneous hypertensive rats (SHR) are an established model of genetic hypertension. Vascular smooth muscle cells (VSMC) from SHR proliferate faster than those of control rats (Wistar-Kyoto rats; WKY). We tested the hypothesis that induction of heme oxygenase (HO)-1 induced by aprotinin inhibits VSMC proliferation through cell cycle arrest in hypertensive rats. Aprotinin treatment inhibited VSMC proliferation in SHR more than in normotensive rats. These inhibitory effects were associated with cell cycle arrest in the G1 phase. Tin protoporphyrin IX (SnPPIX) reversed the anti-proliferative effect of aprotinin in VSMC from SHR. The level of cyclin D was higher in VSMC of SHR than those of WKY. Aprotinin treatment downregulated the cell cycle regulator, cyclin D, but upregulated the cyclin-dependent kinase inhibitor, p21, in VSMC of SHR. Aprotinin induced HO-1 in VSMC of SHR, but not in those of control rats. Furthermore, aprotinin-induced HO-1 inhibited VSMC proliferation of SHR. Consistently, VSMC proliferation in SHR was significantly inhibited by transfection with the HO-1 gene. These results indicate that induction of HO-1 by aprotinin inhibits VSMC proliferation through cell cycle arrest in hypertensive rats.     

表没食子儿茶素没食子酸酯通过下调表皮生长因子受体发挥抑制喉癌细胞的作用机制研究

目的 探究表没食子儿茶素没食子酸酯(epigallocatechin-3-gallate,EGCG)抑制喉癌细胞的作用机制。方法 利用Western blotting检测喉癌细胞株AMC-HN-8、TU686和TU212中表皮生长因子受体(epidermal growth factor receptor,EGFR)的表达,并采用CCK-8法检测西妥昔单抗和EGCG对3种喉癌细胞的抑制作用;构建含有EGFR启动子以及Luc报告基因的慢病毒载体并感染TU686细胞,获得EGFR启动子调控表达荧光素酶的TU686-EGFR-Luc报告基因细胞系,检测EGCG处理后的荧光素酶活性;利用流式细胞术检测EGCG作用后的喉癌细胞的细胞周期和凋亡情况,并用Western blotting检测分析EGFR及下游信号通路分子ERK的表达与活化、细胞周期相关分子P53及P27、凋亡相关分子BCL2及PARP、自噬相关指标LC3A/B的水平情况。结果 喉癌细胞株对西妥昔单抗不敏感,但EGCG能有效抑制喉癌细胞的生长;EGCG能有效抑制EGFR启动子的转录活性;在亚IC₅₀剂量的EGCG作...     

Cell Cycle Arrest and Apoptosis Induction by an Anticancer Chalcone Epoxide

Safe and effective chemotherapeutic agents for the treatment of pancreatic cancer remain elusive. We found that chalcone epoxides (1,3‐diaryl‐2,3‐epoxypropanones) inhibited growth in two pancreatic cancer cell lines, BxPC‐3 and MIA PaCa‐2. Three compounds were active, with GI₅₀ values of 5.6 to 15.8 µM. Compound 4a , 1,3‐bis‐(3,4,5‐trimethoxyphenyl)‐2,3‐epoxypropanone, had an average GI₅₀ of 14.1 µM in the NCI 60‐cell‐line panel. To investigate the mode of action, cell cycle analyses of BxPC‐3 cells were carried out. Treatment of cells with 50 µM 4a resulted in dramatic accumulation at G2/M (61% after 12 h for 4a vs. 15% for untreated cells). The cells rapidly entered apoptosis. After 12 h, 26% of cells treated with 50 µM 4a had entered apoptosis vs. 4% for cells treated with 100 µM etoposide and 2% for untreated cells. Compound 4a interfered with paclitaxel enhancement of tubulin polymerization, suggesting microtubules as the site of action. Reaction of thiol nucleophiles with 4a under basic conditions resulted in epoxide ring‐opening and retroaldol fragmentation, yielding alkylated thiol. MALDI mass spectrometry showed that retroaldol reaction occurred upon treatment of β‐tubulin with 4a . The site of alkylation was identified as Cys³⁵⁴. Chalcone epoxides warrant further study as potential agents for treatment of cancer.     

阿片生长因子抑制乳腺癌细胞生长的研究

目的:探讨阿片生长因子(OGF)对MCF-7人乳腺癌细胞生长的影响。方法:细胞计数观察OGF、阿片生长因子受体(OGFr)拮抗剂纳洛酮(Naloxone)组及对照组细胞数的差别;MTT实验观察应用OGF、Naloxone及OGF联合Naloxone(OGF+Naloxone)细胞增殖抑制率的变化;流式细胞术(FCM)细胞周期分析OGF、Naloxone对MCF-7细胞生长的影响。结果:细胞计数显示,OGF处理组细胞数明显低于Naloxone处理组及对照组(P<0.01),而后2组细胞数差异无统计学意义(P>0.05);MTT实验显示,OGF处理组细胞增殖抑制率明显高于Naloxone处理组及OGF+Naloxone处理组(P<0.01),而后2组差异无统计学意义(P>0.05);OGF处理组MCF-7细胞G0/G1期分数明显高于Naloxone处理组及对照组(P<0.01),而后2组差异无统计学意义(P>0.05)。结论:OGF能抑制MCF-7人乳腺癌细胞的生长。OGFr拮抗剂能阻断这种作用。OGF阻断细胞周期于G0/G1期。     

姜黄素对Tca8113细胞生长、增殖抑制作用的实验研究

目的观察中药有效成分姜黄素对人舌鳞癌Tca8113细胞株生长、增殖的抑制作用。方法将Tca8113细胞培养于普通的RPM I-1640培养基中,实验组用含有不同浓度姜黄素(5μmol/L,10μmol/L,20μmol/L,40μmol/L)的培养基进行培养,采用倒置显微镜观察细胞形态的变化,MTT法检测其生长抑制效应。结果随着姜黄素浓度升高与作用时间的增加,其对细胞的生长、增殖抑制作用明显增强,在倒置显微镜下观察可见细胞生长增殖变慢、细胞形态变圆、变小,脱壁细胞越来越多,漂浮在培养基中。MTT法检测结果显示姜黄素对细胞抑制效应有浓度、时间依赖性。结论姜黄素能明显抑制Tca8113细胞的增殖,其抑制效应与姜黄素浓度、作用时间有依赖关系。     

茵陈素对肺癌细胞增殖和细胞周期的影响

目的 :探讨茵陈素对肺癌细胞增殖和细胞周期的影响。方法 :应用光镜、四氮甲唑蓝 (MTT)方法和流式细胞术分析茵陈素对肺癌细胞形态学、生长和细胞周期的变化。结果 :茵陈素能抑制肺癌细胞的增殖 ,呈剂量依赖性 ,以160μg/ml抑制作用最明显 ,抑制率达52 4 %。80μg/ml时 ,S期和G2/M期细胞比例开始下降 ,细胞被阻滞于G0/G1 期 ,不能进入S期及G2/M期 ,增殖指数明显下降。结论 :茵陈素在体外对肺癌细胞具有抑制作用 ,通过抑制DNA合成 ,将细胞阻滞于G0/G1 期来抑制细胞增殖。     

华蟾素注射液对人肝癌HepG-2细胞增殖及周期的影响

目的探讨华蟾素注射液对人肝癌HepG-2细胞增殖及周期的影响。方法应用噻唑蓝还原法(MTT)检测华蟾素注射液对HepG-2细胞增殖的影响;应用流式细胞术(FCM)检测HepG-2细胞周期分布;采用逆转录-多聚酶链反应技术(RT-PCR)检测华蟾素注射液对HepG-2细胞CyclinA和CDK2 mRNA表达水平的影响;应用比色定量法检测华蟾素注射液对HepG-2细胞内CDK2及CyclinA活性的影响。结果华蟾素注射液可以抑制HepG-2细胞增殖,其抑制作用具有时间和剂量依赖性;可将HepG2细胞阻滞于S期;抑制HepG-2细胞CDK2、CyclinAmRNA水平表达;使HepG-2细胞CyclinA、CDK2活性降低。结论华蟾素注射液能够抑制人肝癌HepG-2细胞增殖,并将细胞阻滞于S期,诱导细胞凋亡,机制可能是通过影响CyclinA、CDK2活性,下调CDK2、CyclinAmRNA水平表达实现的。     

CIB1下调表达对U87胶质瘤细胞增殖和细胞周期的影响

目的 探讨钙整合素结合蛋白1(CIB1)下调表达对U87胶质瘤细胞增殖和周期调节的作用.方法 体外培养U87胶质瘤细胞,通过感染携带siCIB的pGV-siCIB1慢病毒获得CIB1下调表达的U87胶质瘤细胞,将细胞分为pGV-siCIB感染组、对照慢病毒感染组和对照组,采用甲基噻唑基四唑检测细胞增殖情况,流式细胞术检测各组细胞凋亡和细胞周期的改变,定量反转录聚合酶链反应、蛋白免疫印迹法检测U87胶质瘤细胞相关基因和蛋白表达情况.结果pGV-siCIB1感染U87细胞的最适感染复数值为5.siCIB1感染组CIB1 mRNA和蛋白表达低于对照慢病毒感染组和对照组(P<0.05).pGV-siCIB1感染组FOXO1、MDM2 mRNA及CyclinD1、Bcl-2 mRNA和蛋白、p-AKT蛋白表达水平低于对照慢病毒感染组,而Bax、p53、Caspase3 mRNA和蛋白表达水平高于对照慢病毒感染组(P<0.05,P<0.01).pGV-siCIB1感染组U87胶质瘤细胞抑制率、凋亡率与对照慢病毒感染组相比显著增加,与对照组和对照慢病毒感染组相比,G0/G1期细胞增加,S期细胞减少(P<0.05).结论 CIB1下调表达抑制胶质母细胞瘤的生长,促进细胞凋亡. AKT信号通路可能是CIB1发挥作用的途径之一,提示CIB1有可能作为胶质瘤靶向治疗的靶点.     

Podophyllotoxin Induces ROS-Mediated Apoptosis and Cell Cycle Arrest in Human Colorectal Cancer Cells via p38 MAPK Signaling

Podophyllotoxin (PT), a lignan compound from the roots and rhizomes of Podophyllum peltatum, has diverse pharmacological activities including anticancer effect in several types of cancer. The molecular mechanism of the anticancer effects of PT on colorectal cancer cells has not been reported yet. In this study, we sought to evaluate the anticancer effect of PT on human colorectal cancer HCT116 cells and identify the detailed molecular mechanism. PT inhibited the growth of cells and colony formation in a concentration-dependent manner and induced apoptosis as determined by the annexin V/7-aminoactinomycin D double staining assay. PT-induced apoptosis was accompanied by cell cycle arrest in the G2/M phase and an increase in the generation of reactive oxygen species (ROS). The effects of PT on the induction of ROS and apoptosis were prevented by pretreatment with N-acetyl-L-cysteine (NAC), indicating that an increase in ROS generation mediates the apoptosis of HCT116 cells induced by PT. Furthermore, Western blot analysis showed that PT upregulated the level of phospho (p)-p38 mitogen-activated protein kinase (MAPK). The treatment of SB203580, a p38 inhibitor, strongly prevented the apoptosis induced by PT, suggesting that PT-induced apoptosis involved the p38 MAPK signaling pathway. In addition, PT induced the loss of mitochondrial membrane potential and multi-caspase activation. The results suggested that PT induced cell cycle arrest in the G2/M phase and apoptosis through the p38 MAPK signaling pathway by upregulating ROS in HCT116 cells.     

骨碎补总黄酮对大鼠牙髓干细胞增殖和细胞周期的影响

摘要 目的 探讨骨碎补总黄酮对大鼠牙髓干细胞（DPSCs）增殖和细胞周期的影响。方法采用组织块消化法获得大鼠牙髓细胞,克隆化分离培养大鼠DPSCs并进行鉴定。以含0.01,0.05和0.10 g·L－1骨碎补总黄酮的培养基分别培养大鼠DPSCs,采用噻唑蓝（MTT）比色法检测各组细胞的增殖情况,流式细胞术检测各组细胞周期的变化。结果经单克隆化分离培养得到的DPSCs细胞CD44、CD29和Stro 1均呈阳性表达。骨碎补总黄酮组DPSCs增殖速度较对照组加快（P＜0.05）,且随骨碎补总黄酮浓度的增加而升高。流式细胞术分析表明S期细胞比例明显多于对照组（P＜0.05）,G0/G1期细胞明显减少（P＜0.05）,且表现出剂量依赖性。 结论骨碎补总黄酮对大鼠DPSCs增殖具有促进作用,这一作用可能是通过促进DPSCs从G0/G1进入S期来实现。     

染料木素对人宫颈癌Siha细胞增殖凋亡和周期的影响

［摘要］目的探讨染料木素对人宫颈癌Siha细胞增殖、凋亡和周期的影响及机制。方法50 mol&#8226;mL 1染料木素处理Siha细胞,用噻唑蓝（MTT）法检测细胞生长抑制率,用流式细胞术（FCM）检测细胞凋亡、周期及周期蛋白cyclin A和cyclin B表达的变化。结果染料木素作用于Siha细胞后,增殖抑制率比对照组明显升高（P＜0.05）;染料木素处理48 h后,实验组凋亡率较对照组升高,分别为（67.45±1.54）%和（45.37±1.65）%（P＜0.01）。染料木素处理后的Siha细胞G2/M期的细胞比例显著上升,由（9.55±0.71）%升至（79.54±1.09）%（P＜0.01）;cyclin A和cyclin B表达上调,分别由（1.84±0.11）%升至（37.38±0.71）%（P＜0.01）,由（69.44±1.84）%升至（97.70±1.20）%（P＜0.01）。结论染料木素在体外可有效抑制人宫颈癌细胞生长,其抗肿瘤机制可能是上调cyclin A和cyclin B蛋白表达和引起G2/M期细胞周期阻滞。     

绵毛胡桐内酯对人口腔上皮癌KB细胞端粒酶的影响

目的:探讨绵毛胡桐内酯(Calanolide)对KB细胞生长抑制作用及其对端粒酶活性和细胞周期的影响。方法:采用四甲基偶氮唑蓝(MTT)法检测Calanolide对体外培养的KB细胞增殖的抑制作用,TRAP-PCR-ELISA方法检测在Calanolide作用后KB细胞端粒酶活性的变化,用流式细胞仪分析细胞周期的改变。结果:Calanolide在10~50mg/L剂量范围内对KB细胞有抑制作用,且呈剂量依赖关系(P<0.05);Calanolide作用后端粒酶活性出现抑制,且各给药组随Calanolide浓度增加抑制作用显著增强(P<0.01),同一浓度随作用时间延长,抑制作用逐渐增强(P<0.05);KB细胞的G2/M期细胞含量明显增高(P<0.01)。结论:Calanolide对肿瘤细胞的端粒酶活性有抑制作用。     

聚维酮对人膀胱癌T24细胞的抑制作用研究

目的 探讨聚维酮(PVP)对人膀胱癌T24细胞的抑制作用。 方法 采用MTT法检测PVP对T24细胞生长的抑制作用，流式细胞仪检测PVP对T24细胞周期的影响和黏附作用。结果 2.5%PVP作用24和72 h，对人膀胱癌T24细胞生长抑制率分别为（15.11±2.36）%和（49.57±7.07）%；浓度为7.5%时24和72 h抑制率分别（35.42±5.55）%和（79.66±19.92）%。5.0%PVP作用24和72 h时，细胞G0/G1期所占比例分别为（74.17±0.91）%和（46.69±3.76）%；G2/M期细胞所占比例分别为（14.63±0.47）%和（41.88±1.50）%。PVP能提高抗鼠IgG1对T24细胞的黏附作用。结论 PVP能通过诱导人膀胱癌T24细胞周期阻滞于G2/M期和作为化疗药的黏附性载体而抑制癌细胞的生长增殖。     

Rosiglitazone Inhibits Cell Proliferation by Inducing G1 Cell Cycle Arrest and Apoptosis in ADPKD Cyst‐Lining Epithelia Cells

Abstract: Abnormal proliferation is an important pathological feature of autosomal dominant polycystic kidney disease (ADPKD). Many drugs inhibiting cell proliferation have been proved to be effective in slowing the disease progression in ADPKD. Recent evidence has suggested that peroxisome proliferator‐activated receptor γ (PPARγ) ligands have anti‐neoplasm effects through inhibiting cell growth and inducing cell apoptosis in various cancer cells. In the present study, we examined the expression of PPARγ in human ADPKD kidney tissues and cyst‐lining epithelial cell line, and found that the expression of PPARγ was greater in ADPKD kidney tissues and cyst‐lining epithelial cell line than in normal kidney tissues and human kidney cortex (HKC) cell line. Rosiglitazone inhibited significantly proliferation of cyst‐lining epithelial cells in a concentration‐ and time‐dependent manner. These effects were diminished by GW9662, a specific PPARγ antagonist. Cell cycle analysis showed a G0/G1 arrest in human ADPKD cyst‐lining epithelial cells with rosiglitazone treatment. Analysis of cell cycle regulatory proteins revealed that rosiglitazone decreased the protein levels of proliferating cell nuclear antigen, pRb, cyclin D1, cyclin D2 and Cdk4 but increased the levels of p21 and p27 in a dose‐dependent manner. Rosiglitazone also induced apoptosis in cyst‐lining epithelial cells, which was correlated with increased bax expression and decreased bcl‐2 expression. These results suggest PPARγ agonist might serve as a promising drug for the treatment of ADPKD.     

Synthetic Homoisoflavane Derivatives of Cremastranone Suppress Growth of Colorectal Cancer Cells through Cell Cycle Arrest and Induction of Apoptosis

Colorectal cancer is diagnosed as the third most prevalent cancer; thus, effective therapeutic agents are urgently required. In this study, we synthesized six homoisoflavane derivatives of cremastranone and investigated their cytotoxic effects on the human colorectal cancer cell lines HCT116 and LoVo. We further examined the related mechanisms of action using two of the potent compounds, SH-19027 and SHA-035. They substantially reduced the cell viability and proliferation in a dose-dependent manner. Treatment with SH-19027 and SHA-035 induced cell cycle arrest at the G2/M phase and increased expression of p21 both of which are implicated in cell cycle control. In addition, the apoptotic cell population and apoptosis-associated marker expression were accordingly increased. These results suggest that the synthesized cremastranone derivatives have anticancer effects through the suppression of cell proliferation and induction of apoptosis. Therefore, the synthesized cremastranone derivatives could be applied as novel therapeutic agents against colorectal cancer.     

小檗胺对视网膜母细胞瘤HXO-RB44细胞增殖的抑制作用

目的:探讨小檗胺对视网膜母细胞瘤HXO-RB44细胞增殖和细胞周期的影响.方法:体外培养视网膜母细胞瘤HXO-RB44细胞,四甲基偶氮唑蓝(MTT)法测定0、2、4、8、16、32 mg/L小檗胺作用24、48和72 h后对HXO-RB44细胞增殖的抑制率,流式细胞仪检测0、4、8、16 mg/L小檗胺作用HXO-RB44细胞24h后的细胞周期.结果:随着小檗胺浓度的增加和作用时间的延长,其对HXO-RB44抑制率逐渐增加,作用24、48、72 h的IC50分别为25.26、10.94和6.25mg/L.流式细胞分析显示,与空白对照组比较,小檗胺可显著抑制细胞周期,使G2/M期细胞增多(P＜0.01).结论:小檗胺在体外可抑制视网膜母细胞瘤HXO-RB44细胞的增殖,并可诱导G2/M期阻滞,可能成为一种有效的抗视网膜母细胞瘤药物.     

阿托伐他汀对低氧环境下人脐静脉内皮细胞增殖与细胞周期的影响

目的探讨阿托伐他汀对低氧环境下人脐静脉内皮细胞(HUVECs)增殖和细胞周期的影响。方法将培养的HUVECs随机平均分为5组,每组8孔。正常对照组给予血清DMEM液培养12 h;低氧模型组置于低氧装置中用无血清DMEM液培养12 h;低、中、高浓度给药组均置于低氧装置中,分别用含0.05,0.10,0.20 mmol.L-1阿托伐他汀钙的无血清DMEM液培养12 h。采用MTT法测定细胞增殖情况,流式细胞术分析各组不同周期细胞所占比例。结果低氧模型组细胞增殖被明显抑制。在低氧环境下分别加入阿托伐他汀后,细胞增殖过程被明显促进,与低氧模型组相比,各浓度给药组差异有显著性或极显著性(P<0.05或P<0.01),但药物浓度与效应呈非线性关系,其中中浓度组促增殖作用最强,而高浓度组促增殖作用明显减弱。给予不同浓度阿托伐他汀干预后,HUVECs细胞周期中S期细胞显著增多,G0/G1期细胞所占比例下降。结论适当浓度的阿托伐他汀对低氧环境下HUVECs的增殖和DNA的合成有促进作用,阿托伐他汀在缺血心肌新生血管形成过程中可能具有一定作用。     

Gallic Acid Hindered Lung Cancer Progression by Inducing Cell Cycle Arrest and Apoptosis in A549 Lung Cancer Cells via PI3K/Akt Pathway

This study elucidates the anti-cancer potential of gallic acid (GA) as a promising therapeutic agent that exerts its effect by regulating the PI3K/Akt pathway. To prove our research rationale, we used diverse experimental methods such as cell viability assay, colony formation assay, tumor spheroid formation assay, cell cycle analysis, TUNEL assay, Western blot analysis, xenograft mouse model and histological analysis. Treatment with GA inhibited cell proliferation in dose-dependent manner as measured by cell viability assay at 48 h. GA and cisplatin (CDDP) also inhibited colony formation and tumor spheroid formation. In addition, GA and CDDP induced apoptosis, as determined by the distribution of early and late apoptotic cells and DNA fragmentation. Western blot analysis revealed that inhibition of the PI3K/Akt pathway induced upregulation of p53 (tumor suppressor protein), which in turn regulated cell cycle related proteins such as p21, p27, Cyclin D1 and E1, and intrinsic apoptotic proteins such as Bax, Bcl-2 and cleaved caspase-3. The anti-cancer effect of GA was further confirmed in an in vivo mouse model. Intraperitoneal injection with GA for 4 weeks in an A549-derived tumor xenograft model reduced the size of tumor mass. Injection of them downregulated the expression of proliferating cell nuclear antigen and p-Akt, but upregulated the expression of cleaved caspase-3 in tumor tissues. Taken together, these results indicated that GA hindered lung cancer progression by inducing cell cycle arrest and apoptosis, suggesting that GA would be a potential therapeutic agent against non-small cell lung cancer.     

三氧化二砷联合热疗对人食管癌细胞株EC-1增值和细胞周期的影响

摘要：目的 探讨三氧化二砷(AS203) 联合热疗对人食管癌细胞株EC-1增殖的抑制作用及机制。方法 经AS203注射液联合热疗处理EC-1细胞后采用MTT法测定细胞的增殖抑制效应; 应用流式细胞术检测细胞周期变化,TUNEL法观察细胞凋亡。结果:与AS203单药或单用热疗相比, AS203与热疗联合应用后可显著抑制EC-1细胞增殖和诱导细胞凋亡, 并使细胞S期和G0/G1期比例明显降低, G2 /M 期明显升高。结论:AS203联合热疗具有协同抗食管癌作用,其机制可能与联合应用后增强诱导食管癌细胞凋亡、细胞周期特异性治疗与细胞周期调控剂联合增效有关。     

小檗胺对大鼠骨肉瘤UMR-106细胞增殖的抑制作用

目的:探讨小檗胺体外对大鼠骨肉瘤UMR-106细胞增殖的抑制作用及机制.方法:0、2、4、8、16、32mg/L小檗胺作用UMR-106细胞24、48、72 h后,采用四甲基偶氮唑蓝(MTT)比色法检测小檗胺对UMR-106细胞增殖的抑制作用;0、4、8、16 mg/L小檗胺作用UMR-106细胞24 h后,Hoechst33258染色激光共聚焦扫描显微镜观察细胞的形态学变化;Annexin V/碘化丙啶(PI)荧光标记流式细胞术(FCM)检测细胞凋亡率;PI荧光标记FCM检测细胞周期变化.结果:小檗胺以剂量依赖方式显著抑制UMR-106细胞的增殖(P＜0.01),其作用24、48、72 h的半数抑制浓度(IC50)分别为24.69、8.03和3.54 mg/L.小檗胺处理组可见核固缩和凋亡小体.空白对照组和小檗胺4、8、16 mg/L处理组的细胞凋亡率分别为(1.64±0.29)％、(3.58±0.31)％、(6.27±0.47)％和(11.27±1.09)％,与空白对照组比较,差异有统计学意义(P＜0.01);同时,小檗胺可以诱导细胞坏死;此外,与空白对照组比较,小檗胺4、8、16 mg/L处理组UMR-106细胞的G0/G1期细胞比例增高,而S期和G2/M期细胞比例呈降低趋势(P＜0.01).结论:小檗胺体外能够抑制骨肉瘤UMR-106细胞增殖,其机制与诱导细胞凋亡、坏死和G0/G1期阻滞有关.