美洲大蠊多肽提取物对SMMC-7721细胞凋亡及Bcl-2和Bax蛋白表达的影响

目的：研究美洲大蠊多肽提取物诱导人肝癌细胞SMMC-7721凋亡及其分子机制。方法：采用不同质量浓度的美洲大蠊多肽提取物作用于SMMC-7721,以Cell Counting Kit-8（CCK-8）法检测细胞抑制率;Hoechst33342/PI与Annexin V-FITC/PI双染法相结合检测SMMC-7721细胞的凋亡;蛋白免疫印迹（Western blotting）法检测细胞凋亡相关因子Bcl-2和Bax蛋白表达。结果：不同质量浓度的美洲大蠊多肽提取物可抑制SMMC-7721细胞的增殖,诱导其凋亡,呈一定的量效关系;Western Blot法显示Bax表达增多,Bcl-2蛋白表达减少,Bcl-2/Bax比值降低。结论：美洲大蠊多肽提取物可明显诱导SMMC-7721细胞凋亡,抑制其增殖,其机制可能与下调Bcl-2蛋白表达,上调Bax蛋白表达,降低Bcl-2/Bax比值有关。     

牡荆素对人肝细胞癌SMMC-7721细胞的增殖抑制作用及其机制的影响

目的: 研究牡荆素(vitexin)对人肝癌细胞SMMC-7721的增殖抑制作用, 并初步探讨其作用机制。方法: 体外培养人肝癌细胞SMMC-7721, 分别采用MTT法和Hoechst33258核染色法检测牡荆素对人肝癌细胞SMMC-7721活力的影响以及观察细胞形态学变化;流式细胞仪检测细胞凋亡率和线粒体膜电位(ΔΨm) 变化;蛋白免疫印迹法检测p53、Bcl-2、Bax等相关凋亡蛋白水平的表达情况。结果: 牡荆素培养人肝癌细胞SMMC-7721 48, 72, 96 h后能明显抑制细胞增殖, 呈时间-剂量依赖性(P<0.05), 其IC₅₀分别是150.37, 116.24, 90.19 μmol·L^-1。牡荆素作用于人肝癌细胞SMMC-7721 72 h后, 以浓度依赖性方式增加细胞凋亡率、降低线粒体膜电位(ΔΨm) 以及上调p53、Bax、Caspase-3等相关促凋亡蛋白的表达, 下调Bcl-2抗凋亡蛋白的表达。结论: 牡荆素能抑制人肝癌细胞SMMC-7721增殖诱导凋亡, 呈时间-剂量依赖性, 其作用机制可能通过依赖P53途径下调Bcl-2, 上调Casepase-3、Bax、P53、PARP等基因表达, 进而诱导凋亡有关。     

新型金属铜络合物对SMMC-7721细胞增殖与凋亡的影响

目的研究新型金属铜络合物(N-Cu)在体外对人肝癌SMMC-7721细胞增殖与凋亡的影响及其作用机制。方法将不同浓度的N-Cu(0.3～24μmol.L-1)作用于体外培养的SMMC-7721细胞,应用MTT法检测细胞生长抑制率,FCM法检测细胞周期及凋亡率,RT-PCR和Western blot法检测细胞中Bcl-2、Bax、Caspase-3 mRNA和蛋白表达的变化。结果 N-Cu可明显抑制SMMC-7721细胞的增殖,呈明显的量效与时效关系。随着药物浓度的增加,G0/G1期的细胞比率上升,G2/M和S期细胞比率下降,并促进凋亡率增加。N-Cu可上调细胞中Bax、Caspase-3基因及蛋白的表达,抑制Bcl-2基因及蛋白的表达,且均呈剂量依赖性。结论一定浓度的N-Cu可抑制SMMC-7721细胞的增殖并诱导其凋亡,阻滞细胞周期于G0/G1期。上调Bax、Caspase-3基因及蛋白的表达,降低Bcl-2/Bax比值,可能是其诱导细胞凋亡的重要机制。     

Cytotoxic effects and pro-apoptotic mechanism of TBIDOM, a novel dehydroabietylamine derivative, on human hepatocellular carcinoma SMMC-7721 cells

We have investigated the antiproliferative effects of TBIDOM (N-(4-(2,2,2-trifluoroethyl) benzylidene) (7-isopropyl-1,4a-dimethyl-1,2,3,4,4a,9,10,10a-octahydrophenanthren-1-yl) meth-anamine) and have explored its possible mechanisms on human hepatocellular carcinoma SMMC-7721 cells. The proliferative status of cells treated with TBIDOM was measured by the colorimetric MTT assay. Cellular apoptosis was analysed using Hoechst 33342 staining and flow cytometry. Reduction of mitochondrial membrane potential (Delta psi(m)) was also detected by flow cytometry. Western blotting assay was used to evaluate the release of cytochrome c and expression of p53, Bcl-2 and Bax proteins. It was shown that TBIDOM displayed a significant inhibitory effect on growth of SMMC-7721 cells in a dose- and time-dependent manner. Hoechst 33342 staining and flow cytometry analysis showed an increase of apoptosis rate and decrease of mitochondrial membrane potential after SMMC-7721 cells were exposed to TBIDOM for 24 h. Pretreatment of SMMC-7721 cells with TBIDOM significantly induced a decrease of Bcl-2 protein expression and an increase of caspase-3 activity and Bax protein expression. The results indicated that TBIDOM could effectively inhibit proliferation by induction of apoptosis and could be a promising candidate in the development of a novel class of antitumour agent.     

Piperonal ciprofloxacin hydrazone induces growth arrest and apoptosis of human hepatocarcinoma SMMC-7721 cells

Aim:

To investigate the cytotoxic effects of piperonal ciprofloxacin hydrazone (QNT4), a novel antibacterial fluoroquinolone derivative, against human hepatocarcinoma SMMC-7721 cells.

Methods:

Human hepatocarcinoma cells (SMMC-7721), human breast adenocarcinoma cells (MCF-7) and human colon adenocarcinoma cells (HCT-8) were tested. The effects of QNT4 on cell proliferation were examined using MTT assay. Cell apoptosis was determined using Hoechst 33258 fluorescence staining, TUNEL assay and agarose gel electrophoresis. The topoisomerase II activity was measured using agarose gel electrophoresis with the DNA plasmid pBR322 as the substrate. Mitochondrial membrane potential (Δψm) was measured using a high content screening imaging system. Protein expression of caspase-9, caspase-8, caspase-3, p53, Bcl-2, Bax, and cytochrome c was detected with Western blot analysis.

Results:

Treatment with QNT4 (0.625–10 μmol/L) potently inhibited the proliferation of the cancer cells in time- and dose-dependent manners (the IC₅₀ value at 24 h in SMMC-7721 cells, MCF-7 cells and HCT-8 cells was 2.956±0.024, 3.710±0.027, and 3.694±0.030 μmol/L, respectively). Treatment of SMMC-7721 cells with QNT4 (0.2146, 2.964, and 4.600 μmol/L) for 24 h dose-dependently increased the percentage of apoptotic cells, elicited characteristic DNA “ladder” bands, and decreased the mitochondrial membrane potential. QNT4 dose-dependently increased topoisomerase II-mediated DNA breaks while inhibiting DNA relegation, thus keeping the DNA in fragments. Treatment of SMMC-7721 cells with QNT4 significantly increased cytochrome c in the cytosol, and decreased cytochrome c in the mitochondrial compartment. QNT4 (3–7.39 μmol/L) significantly increased the protein expression of p53, Bax, caspase-9, caspase-3, and the cleaved activated forms of caspase-9 and caspase-3 in SMMC-7721 cells. In contrast, the expression of Bcl-2 was decreased, while caspase-8 had no significant change.

Conclusion:

QNT4 induced the apoptosis of SMMC-7721 cells via inhibiting topoisomerase II activity and modulating mitochondrial-dependent pathways.     

Synergistic effect of combining paeonol and cisplatin on apoptotic induction of human hepatoma cell lines

Aim： To investigate whether paeonol （Pae） has synergistic effects with cisplatin （CDDP） on the growth-inhibition and apoptosis-induction of human hepatoma cell lines HepG2 and SMMC-7721. Methods： The cytotoxic effect of drugs was measured by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyl-tetrazolium bromide assay. The coefficient of drug interaction was used to analyze the nature of drug interactions. Morphological changes were observed by acridine orange fluorescence staining. Cell cycle and the apoptosis rate were detected by flow cytometry. Bcl-2 and Bax expression were assayed by immunohistochemical staining. Results： Pae or CDDP had antiproliferative effect on the 2 cell lines in a dose-dependent manner, with different sensitivities to drugs. More interestingly, a synergistic inhibitory effect on the viability of the 2 cell lines was observed after treatment with a combination of Pae （15.63, 31.25, and 62.5 mg/L） with various concentrations of CDDP. Further study showed typical morphological changes of apoptosis if the cells were exposed to the two agents for 24 h. The apoptotic rate of the cells with combination treatment was significantly higher than that of cells treated with Pae or CDDP alone. The expression of Bcl-2 decreased and that of Bax increased in the treated groups, especially in the combination group, with the ratio of Bcl-2/Bax decreasing correspondingly. Additionally, a combination of Pae with CDDP resulted in a stronger S phase arrest, compared with Pae or CDDP alone. Conclusion： Pae, in combination with CDDP, had a significantly synergistic growth-inhibitory and apoptosis-inducing effect on the 2 human hepatoma cell lines, which may be useful in hepatoma treatment.     

Mechanism of apoptosis induced by a polysaccharide, from the loach Misgurnus anguillicaudatus (MAP) in human hepatocellular carcinoma cells

The biological activities of the polysaccharide have attracted more and more attention in the biochemical and medical areas due to their anti-cancer effects. To estimate the anti-tumor mechanism of MAP, a novel polysaccharide from the loach, Misgurnus anguillicaudatus, the apoptosis effects of the polysaccharide on the human hepatocellular carcinoma cells (SMMC-7721 cells) were studied. The present studies showed that MAP could induce cell apoptosis which was closely accompanied with an increase of intracellular-free calcium concentration ([Ca2+]i), the enhancement of reactive oxygen species (ROS) level, dissipation of mitochondria membrane potential (MMP), up-regulation of p53 mRNA, increase expression of Bax mRNA, and decrease expression of Bcl-2 mRNA. These results suggested that cell apoptosis induced by MAP mainly was mediated by mitochondrial pathways, not involved death receptors (DRs) pathways. The mechanism possibly is that MAP acts on mitochondria and boosts ROS, ROS mediates a release of Ca2+ from the intracellular Ca2+ pool, increasing [Ca2+]i targets the cells a start-up of the apoptosis program. However, further research on the molecular mechanisms of MAP effecting on the cells' mitochondria is necessary.     

Induction of apoptosis by chelerythrine chloride through mitochondrial pathway and Bcl-2 family proteins in human hepatoma SMMC-7721 Cell

The objective of this study was to evaluate the antitumor activity of chelerythrine chloride (CHE) and investigate its potential apoptotic induction mechanism in SMMC-7721 cells. Our results suggested that the proliferation of SMMC-7721 cells was inhibited by CHE in a time and dose dependent manner, with a significant accumulation in S phase, and the cells exhibited typical apoptotic features. Moreover, CHE remarkably induced apoptosis by disruption of the mitochondrial membrane potential, release of Cyt-c, activation of caspase-3, and cleavage of poly-ADP-ribose polymerase in a dose dependent manner. Furthermore, the expression of Bcl-xl was downregulated while Bax and Bid expression was upregulated, and no variation was found for Bcl-2. These results indicated that CHE may play an important role in suppression of tumor growth by inducing apoptosis in human hepatoma cells via the activation of a mitochondrial pathway and regulating the expression of Bcl-2 family proteins.     

In vitro effects on proliferation, telomerase activity and apoptosis of an eremophilanoid sesquiterpene from Senecio oldhamianus maxim in cultured human tumor cell lines

8,11-Dioxol-6-en-9alpha, 10alpha-epoxy-8beta-hydroxyeremophilane (HEM), a new eremophilanoid sesquiterpene, was isolated from Senecio oldhamianus Maxim. Its effects of cytotoxicity, telomerase activity, apoptosis and related genes expression in two human tumor cell lines, human hepatoma cells SMMC-7721 and human oophoroma cells HO-8910, were studied. Hydroxycamptothecine (HCPT) was used as a positive control. The IC50 of cytotoxicity by HEM were 24.9 +/- 2.1 and 19.4 1.6 microM in SMMC-7721 and HO-8910 cells respectively, and 0.35 +/- 0.10 and 0.27 +/- 0.08 microM for HCPT. HEM inhibited telomerase activity with the IC50 35.9 +/- 3.2 microM in SMMC-7721 and 25.6 +/- 2.6 microM in HO-8910 cells, while HCPT had no effect on telomerase activity in both tumor cell lines. HEM 20-30 microM induced apoptosis in SMMC-7721 cells from 5.7% to 18.4% and in HO-8910 cells from 7.6% to 67.1%. While HCPT 0.1-0.5 microM induced apoptosis in SMMC-7721 cells from 6.5% to 13.3% and in HO-8910 cells from 9.9% to 30.9%. HEM 30 microM significantly decreased Bcl-2 protein expression to 58.7% in SMMC-7721 and to 57.6% in HO-8910 cells. While HCPT 0.5 microM significantly decreased Bcl-2 protein expression to 64.3% in SMMC-7721 and to 70.0% in HO-8910 cells. HEM 25 microM and 30 microM significantly increased P53 protein expression 2.3-3.6-fold in SMMC-7721 and 3.0-5.7- fold in HO-8910 cells. While HCPT 0.5 microM significantly increased P53 protein expression 3.3-fold in SMMC-7721 and 2.7-fold in HO-8910 cells. Overall, HCPT exhibited a more potent effect on cytotoxicity and apoptosis in the two tumor cell lines than HEM did. However HEM can inhibit telomerase activity in the two tumor cell lines but HCPT cannot.     

Effect of liquiritigenin,a flavanone existed from Radix glycyrrhizae on pro-apoptotic in SMMC-7721 cells

Liquiritigenin is a flavanone existed in Radix glycyrrhizae. The objective of this study is to explore the effects of liquiritigenin on SMMC-7721 cells and its possible mechanism. The viability of liquiritigenin treat cells was decreased in a dose-dependent manner assayed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenylterazolium bromide (MTT), and apoptotic morphological changes also be observed, such as chromatin condensation and nuclear fragmentation. Assessment of apoptotic cells by flow cytometry indicated that cells fell into apoptosis after 0.4 mM liquiritigenin treatment. In addition, a concomitant time-dependent increase in caspase-3 activity was also observed. The level of p53 protein increased and Bcl-2 protein decreased time-dependently. Further studies found the induction of apoptosis by liquiritigenin was accompanied with the production of reactive oxygen species (ROS), disruption of mitochondrial membrane potential and depletion of antioxidant enzymes. The significant ROS generation was firstly found at 3 h and being time-dependent until 9 h. A time-dependent decrease in membrane potential occurred, and significant loss appeared at 9 h and 12 h. Furthermore, pretreatment of N-acetyl-cysteine (NAC), ROS production and apoptosis induced by liquiritigenin were both suppressed. In sum, this paper indicated the cytotoxicity of liquiritigenin on SMMC-7721 cells may via effect on generation of ROS, later lead to cell apoptosis.     

20(S)-原人参二醇对SMMC-7721细胞体内外作用的研究

目的观察不同剂量的20(S)-原人参二醇(Protopanaxadiol,PPD)在体内外对人肝癌细胞株SMMC-7721抗肿瘤作用。方法建立人肝癌裸鼠皮下移植瘤模型,观察20(S)-原人参二醇的肿瘤抑制作用。MTT比色法检测20(S)-原人参二醇对SMMC-7721细胞的增殖抑制作用,Ho-echst33342核染色观察细胞凋亡形态学改变,采用FITC-An-nexinⅤ/PI双染流式细胞术分析凋亡情况,同时检测Caspase-3活性。结果在体内,PPD可抑制SMMC-7721细胞裸鼠异种移植瘤生长;在体外,PPD对SMMC-7721细胞的增殖具有明显的抑制及诱导其凋亡作用,呈时间和剂量依赖性,Hoechst33342核染色可见凋亡小体,同时伴有Caspase-3活性的增加。结论20(S)-原人参二醇在体内外均可抑制SMMC-7721细胞增殖,并诱导其凋亡,其机制可能通过活化Caspase-3诱导细胞凋亡而发挥抗肿瘤作用。     

p 16 基因对人肝癌细胞的生长抑制作用的初步研究

目的探讨抑癌基因p16对肝癌细胞生长的抑制作用。方法将p16 cDNA亚克隆至pcDNA3.1真核表达载体上,并经脂质体介导转染至人肝癌细胞株SMMC-7721。用MTT法和Western blot分析转染细胞的生长情况。结果成功构建重组表达质粒pcDNA3.1-p16,转染pcDNA3.1-p16的SMMC-7721细胞生长速度受到明显抑制;经Western blot证实,转染后有外源p16蛋白的表达,且伴随Bax上调,Bcl-2和cIAP2的下调。结论重组pcDNA3.1-p16质粒能在人肝癌细胞SMMC-7721内表达,且能抑制SMMC-7721的生长,其机理与诱导肿瘤细胞凋亡相关。     

Mechanism of apoptotosis induced by ortho-topolin riboside in human hepatoma cell line SMMC-7721

The naturally occurring cytokinin, ortho-topolin riboside (oTR), has been recently reported to have a strong anticancer effect. However, the molecular mechanism has not been elucidated. From our research we found that oTR strongly inhibited the proliferation of SMMC-7721 cells inducing apoptosis. After oTR treatment, up-regulation of the protein levels of pro-apoptotic Bax and the down-regulation of the anti-apoptotic proteins, Bcl-2 and Bcl-xL was observed, leading to the loss of mitochondrial membrane potential, the release of cytochrome c from the mitochondria into the cytosol, the downstream activation of caspase-9 and caspase-3, as well as the cleavage of poly ADP-ribose-polymerase (PARP), the effect of apoptosis could be blocked by the pan-specific caspase inhibitor z-VAD-fmk and caspase-9-specific inhibitor z-LEHD-fmk. Moreover, oTR was shown to inhibit the activation of the extracellular signal-regulated kinase-1/2 (ERK_1/2) as well as the Akt pathway. These results suggest that oTR interferes with the mitogen-activated protein kinase (MAPK) and Akt pathways and induces the apoptosis of human SMMC-7721 cells through the activation of intrinsic mitochondria-mediated pathways. However, the apoptosis was completely prevented when cells were treated with A-134974, an inhibitor of adenosine kinase, it indicated that the intracellular phosphorylation of oTR is necessary for its cytotoxic effects to SMMC-7721 cells.     

白花丹醌对人肝癌细胞HepG2、SMMC-7721增殖及其Bax/Bcl-2、Cyclin D1 mRNA表达的影响

目的探索白花丹醌对人肝癌细胞HepG2、SMMC-7721增殖的影响及其影响机制。方法人肝癌细胞HepG2和SMMC-7721分别与白花丹醌共培养,通过显微图像、MTT法检测了白花丹醌对上述两种肝癌细胞增殖情况的影响,利用实时荧光定量PCR(Qpcr)检测其Bax/Bcl-2,Cyclin D1mRNA表达的影响。结果显微照像和MTT法测定都表明白花丹醌能明显地抑制两种肝癌细胞的增殖;Qpcr检测表明,对HepG2和SMMC-7721,白花丹醌能明显上调Bax/Bcl-2mRNA比值(P=0.0017和P=0.00104),同时明显下调Cy-clin D1 mRNA水平(P=0.0287和P=0.0165)。结论白花丹醌能抑制HepG2、SMMC-7721的增殖,其机制与Bax/Bcl-2比值上升和Cyclin D1转录水平下降有关。     

EGCG诱导人肝癌SMMC-7721细胞早期凋亡及基因和蛋白谱的变化研究

目的探讨表没食子儿茶素没食子酸酯(EGCG)诱导人肝癌SMMC-7721细胞早期凋亡的变化规律,以及EGCG作用后SMMC-7721细胞基因及蛋白谱的变化。方法通过MTT法初步筛选EGCG诱导SMMC-7721细胞凋亡的作用浓度,流式细胞Annexin V-FITC/PI法检测EGCG对SMMC-7721细胞增殖的抑制作用和早期凋亡的诱导效应;运用Af-fymetrix U133A2.0人基因组表达谱芯片检测EGCG作用后SMMC-7721细胞基因表达谱的变化,以及SELDI检测EGCG作用后SMMC-7721细胞蛋白图谱的变化,Real-time PCR验证3个表达差异显著基因。结果EGCG诱导SMMC-7721细胞早期凋亡的最佳作用剂量是218.2μmol·L-1,早期凋亡的作用呈剂量依赖性;SMMC-7721细胞经EGCG作用后,表达差异两倍以上的基因共196个,包括上调基因132个和下调基因64个;EGCG作用后表达差异两倍以上的蛋白共43个,包括23个表达上调蛋白,20个表达下调蛋白。Real-time PCR验证DIO2、Id3基因表达与芯片结果一致。结论EGCG有明显的诱导肝癌SMMC-7721细胞早期凋亡的作用,其诱导凋亡作用涉及多基因和多蛋白变化。     

维生素D对过氧化氢诱导MIN6细胞凋亡的保护作用

目的探讨维生素D(vitamin D,VitD)对过氧化氢(hydrogen peroxide,H 2O 2)诱导小鼠胰岛β细胞株MIN6细胞凋亡的保护作用及机制。方法VitD预处理后,用H 2O 2处理MIN6细胞,分别运用CCK-8法、Hoechst 33258荧光染色法、流式细胞术检测MIN6细胞增殖、形态及凋亡百分率。Western blot检测增殖与凋亡相关基因Bax、Bcl-2、Caspase-3以及Cleaved caspase-3的表达。结果H 2O 2呈时间和剂量依赖性抑制MIN6细胞增殖,诱导细胞凋亡,降低Bcl-2表达、增加Bax及Cleaved caspase-3表达,Bcl-2/Bax比值降低,Cleaved caspase-3/caspase-3比值增加;当用VitD预处理后,Bcl-2表达增加,Bax、Cleaved caspase-3表达降低,Bcl-2/Bax比值增加,Cleaved caspase-3/caspase-3比值降低,MIN6细胞活力增加。结论VitD预处理后,通过增加抗凋亡Bcl-2表达,降低促凋亡Bax和Cleaved caspase-3表达,减少由H 2O 2诱导的小鼠胰岛β细胞株MIN6细胞凋亡。     

实时动态法分析七味红花殊胜丸抑制肝癌细胞线粒体代谢

目的：观察七味红花殊胜丸对人肝癌SMMC-7721细胞线粒体代谢酶的影响。方法：运用实时动态法分析七味红花殊胜丸对细胞活性的影响及各给药组不同时间IC₅₀值的变化情况。采用MTT法检测七味红花殊胜丸对SMMC-7721细胞的抑制率;ELISA法检测七味红花殊胜丸对SMMC-7721细胞线粒体代谢和凋亡的影响,Western Blot法检测凋亡蛋白的表达状况。结果：实时动态检测结果提示,七味红花殊胜丸5 mg·mL^-1作用48 h对SMMC-7721细胞的抑制率最高（P<0.01）;ELISA检测结果提示,七味红花殊胜丸能降低SMMC-7721细胞内ATP、ATPase、线粒体呼吸链复合物Ⅰ/Ⅱ/Ⅲ/Ⅳ酶的表达量,影响细胞的能量代谢;升高促凋亡蛋白Bax、Caspase-3和Caspase-9的表达量,降低抗凋亡蛋白Bcl-2的表达量,诱导细胞凋亡。结论：七味红花殊胜丸可通过影响细胞的能量代谢,诱导SMMC-7721细胞凋亡。     

Thapsigargin induces apoptosis when autophagy is inhibited in HepG2 cells and both processes are regulated by ROS-dependent pathway

Thapsigargin (TG), is widely used to induce endoplasmic reticular stress. Treated with TG for a long time, cells suffer the unfolded protein response (UPR) to elude apoptosis, but may activate autophagy. However, the switch between autophagy and apoptosis is unclear. To clarify the key signal for selection of these two protective responses, we studied the correlation of autophagy and apoptosis in HepG2 cells exposed to TG with time. TG induced apoptosis in HepG2 cells was evidenced by typical cell morphological changes and the activation of caspase-12, caspase-9 and caspase-3. Meanwhile, cytochrome c was released following with the dissipation of mitochondrial membrane potential (MMP), and the ratio of Bax/Bcl-2 was increased. TG-induced autophagy was confirmed by the accumulation of MDC, GFP-LC3 staining autophagic vacuoles, and the improved expression of LC3 II and Beclin-1. Additionally, inhibited autophagy via chloroquine (CQ) markedly enhanced the apoptosis induced by TG, which was linked to the Bcl-2 family. Furthermore, TG induced the generation of reactive oxygen species (ROS), and the ROS scavenger effectively suppressed TG-induced apoptosis and autophagy. All these results proved that restraint of autophagy may enhance TG-induced apoptosis through increasing the Bax/Bcl-2 ratio and both processes were regulated by ROS.     

Anticancer effect of two diterpenoid compounds isolated from Annona glabra Linn

INTRODUCTION Traditional Chinese medicine afforded a valuableapproach in the searching for new anticancer drugs.Studies on the pharmacological mechanism and search-ing for new chemical structures from herbal extractfor new anticancer drugs caught great interest[1]. Taxol,isolated from the stem bark of Taxus brevifolia, pro-vided a typical example in this respect. Taxol was rankedas “the most important new drug we have had in can-cer for 15 years”[2]. Annonaceous acetogenius were …