A new acylated flavonoid glycoside from the flowers of Camellia nitidissima and its effect on the induction of apoptosis in human lymphoma U937 cells

From the EtOH extract of the flowers of Camellia nitidissima Chi, a new acylated flavonoid glycoside, quercetin 7-O-(6″-O-E-caffeoyl)-β-d-glucopyranoside (1), has been isolated, together with three known flavonoids: quercetin (2), quercetin 3-O-β-d-glucopyranoside (3), and quercetin 7-O-β-d-glucopyranoside (4). Their structures were elucidated on the basis of spectroscopic analysis. Compound 1 was shown to inhibit proliferation and to induce apoptosis of human lymphoma U937 cells.     

赤芍总苷对大鼠缺血损伤心肌细胞凋亡的保护作用

目的研究赤芍总苷(TPG)对异丙基肾上腺素(ISO)诱导的心肌缺血损伤大鼠细胞凋亡的保护作用及其机制。方法Rona法复制大鼠心肌缺血损伤模型,检测和对比分析正常对照组、ISO损伤组、TPG防治组、TPG治疗组和心得安阳性对照组的心肌细胞早期凋亡率、心肌组织凋亡相关基因Bax、Bcl-2及其蛋白的相对表达量。结果与ISO损伤组比较,TPG防治组和治疗组各项指标均有不同程度的改善,表现为大鼠早期心肌细胞凋亡率和促凋亡基因Bax及其蛋白的表达量明显降低,而抑凋亡基因Bcl-2及其蛋白的表达量有所增高,Bcl-2/Bax蛋白比值明显高于ISO损伤组。结论TPG对ISO诱导的大鼠心肌缺血损伤时的细胞凋亡具有保护作用,药用机制可能与激活Bcl-2基因及其蛋白表达,抑制Bax基因及其蛋白表达,提高Bcl-2/Bax蛋白比值,从而有效抑制心肌细胞凋亡有关。     

管花肉苁蓉苯乙醇苷提取物对血管内皮细胞EA.hy926增殖的抑制和凋亡的诱导作用

目的 研究管花肉苁蓉苯乙醇苷提取物对血管内皮细胞EA.hy926增殖的抑制和凋亡的诱导作用.方法 采用CCK-8法测定细胞增殖的抑制率,用Hoechst33342染色法观察细胞的凋亡形态,采用Annexin V-FITC/PI双染法结合流式细胞仪测定细胞的凋亡率,用Western blot法检测凋亡相关蛋白Bcl-2、Bax的表达情况.结果 与对照组相比,管花肉苁蓉苯乙醇苷提取物能够抑制血管内皮细胞的增殖且呈剂量依赖性,其作用24h时的IC50 =30.61 μg·mL-1;能够增加血管内皮细胞凋亡率,药物组的细胞呈现核浓染和固缩现象,能够降低抗凋亡蛋白Bcl-2的表达、增加促凋亡蛋白Bax的表达、Bcl-2/Bax值显著降低.结论 肉苁蓉苯乙醇苷提取物能够通过诱导血管内皮细胞的凋亡来抑制其增殖,其机制与调控凋亡相关蛋白Bcl-2、Bax的表达有关.     

Molecular mechanisms involved in the adaptive response to cadmium-induced apoptosis in human myelomonocytic lymphoma U937 cells

We examined the molecular mechanisms involved in the adaptive response to cadmium (Cd)-induced apoptosis in human myelomonocytic lymphoma U937 cells. When U937 cells were treated with 50 μM cadmium chloride (CdCl₂) for 12 h, significant apoptosis occurred. This was associated with an increase in intracellular reactive oxygen species (ROS), sustained phosphorylation of JNK, activation of caspase-3, a decrease in Mcl-1 (anti-apoptotic Bcl-2 proteins), and increases in Bim, Noxa and tBid (a pro-apoptotic protein under the Bcl-2 family). No apoptosis occurred when the cells were treated with 1 μM CdCl₂ for 72 h. However, pretreatment with low-dose CdCl₂ dramatically altered the sensitivity of the cells to 50 μM CdCl₂ with inhibition of apoptosis. Concomitantly, there were significant decreases in the generation of intracellular ROS and the activation of JNK. Pretreatment with 1 μM CdCl₂ also attenuated the decrease in Mcl-1 and the increases in Bim, Noxa and tBid induced by 50 μM CdCl₂. In conclusion, pretreatment with low-dose Cd inhibited apoptosis induced by high-dose Cd. The mechanism involves inhibition of intracellular ROS generation and JNK activation, and modulating the balance between the expression of Mcl-1 and its binding partners, Bim, Noxa and tBid.     

苦马豆根和茎中一个新黄酮苷

目的研究苦马豆根和茎的化学成分。方法采用反复硅胶柱色谱、Sephadex LH-20色谱进行化合物的分离,根据波谱数据鉴定化合物结构。结果从95%乙醇提取物正丁醇萃取部分得到8个化合物,鉴定为：异鼠李素-3-O-［6″-(3-羟基-3-甲基戊二酸单酯)-β-D-吡喃葡糖苷］(I)、槲皮苷(II)、正丁基-β-D-吡喃果糖苷(III)、尼克酸(IV)、丁二酸(V)、赤藓醇(VI)、D-甘露醇(VII)和尿嘧啶核苷(VIII)。结论化合物I为新化合物,化合物I-VI均为首次从本属植物中得到。     

雷公藤多苷含药血清对人L02肝细胞株增殖和凋亡的影响

目的 研究雷公藤多苷含药血清对人LD2正常肝细胞株增殖和凋亡的影响.方法 用不同浓度雷公藤多苷含药血清(0%、5%、10%、20%)干预体外培养的人L02肝细胞株48 h后,采用MTT法检测计算L02细胞的生长抑制率,采用流式细胞术检测Bax和Bcl-2蛋白表达.结果 5%、10%、20%的雷公藤多苷含药血清组吸光度值均低于对照组[分别为(0.60±0.09)、(0.51±0.06)、(0.39±0.07)比(0.69±0.05),均P＜0.05].20%雷公藤多苷含药血清抑制作用强于10%含药血清(43%比26%),10%含药血清抑制作用强于5%含药血清[26%比13%],抑制作用具有剂量依赖性.雷公藤多苷含药血清干预后Bax表达增强(P＜0.05)以及Bcl-2表达降低(P＜0.01),并且Bax和Bcl-2的变化具有剂量依赖性.结论 雷公藤多苷含药血清对人L02正常肝细胞株的增殖有抑制作用,并可诱导其凋亡相关蛋白表达发生变化.

Abstract：

Objective To study the efect of tripterygium glycoside drug serum on the proliferation and apoptosis of human heptical cell line L02 cells. Methods In vitro, L02 cells were fed with tripterygium glycoside drug serum at different concentrations (0% , 5% , 10% , 20%) for 48 hours. Cell growth activity was detected by methylthiazoletetrazolium assay; apoptosis related proteins Bax and Bcl-2 were tested by flow cytometry. Results Tripterygium glycoside drug serum significantly suppressed proliferation of L02 cells and the effect of proliferation was dose-dependent. The level of Bax rose and Bcl-2 decreased obviously with by tripterygium glycoside drug serum in L02 cells. Meanwhile the changes of Bax and Bcl-2 were dose-dependent. Conclusion Tripterygium Clycoside drug serum has effects on the proliferation of L02 cells and the changes in Bax and Bcl-2.     

A new drimane sesquiterpenoid glycoside from the seeds of Antiaris toxicaria

A new drimane sesquiterpenoid glycoside, named 7-drimen-3β,11-diol 3-O-β-d-glucopyranoside, was isolated from the 95% EtOH extract of the seeds of Antiaris toxicaria (Pers.) Lesch. The chemical structure was completely elucidated using a combination of 1D and 2D NMR techniques (COSY, HMQC, HMBC, and ROESY) and HR-ESI-MS analysis. The compound showed inhibitory activities toward methicillin-resistant Staphylococcus aureus (MRSA), chronic myelogenous leukemia (K562), and human hepatoma (SMMC-7721) cell lines.     

姜黄素对HL-60细胞的增殖抑制与凋亡诱导的影响

目的研究姜黄素对人原髓细胞白血病HL-60细胞的增殖抑制及凋亡诱导作用,探讨其诱导细胞凋亡的机理。方法应用MTT比色法、细胞荧光染色法和Western blotting检测姜黄素对HL-60细胞的增殖抑制、凋亡诱导以及对HL-60细胞表达Bcl-2、Caspase9和c-myc的影响。结果姜黄素对HL-60细胞的增殖抑制与剂量相关(P<0.05);经姜黄素作用后HL-60细胞的形态差异明显,表现凋亡的特征性变化,而且姜黄素作用后HL-60细胞的Bcl-2和原癌基因c-myc的表达量低于对照组(P<0.05),而Caspase9的表达量则明显高于对照组(P<0.05)。结论姜黄素可有效抑制体外培养的HL-60细胞增殖,其诱导HL-60细胞凋亡的途径可能通过线粒体介导。     

Direct‐oxidative DNA damage and apoptosis induction in different human respiratory cells exposed to low concentrations of sodium chromate

The mechanism of Cr(VI) genotoxicity has still not been elucidated. We used Fpg‐modified comet assay to assess direct‐oxidative DNA damage on human lung (A549) and bronchial (BEAS‐2B) cells exposed to 0.1, 0.5, 1.0 and 10 μm sodium chromate for 0.5, 1 and 4 h. Moreover we evaluated apoptosis by morphological analysis and caspase‐3 activity, also after 24 h. On A549 cells a time‐dependent DNA damage, expressed as tail DNA%, beginning from 0.5 μm was found. For oxidative DNA damage an induction after 30 min to 0.5 μm decreasing with time, and a time‐dependent increase at 10 μm was found, indicating for low Cr(VI) concentration the oxidative stress as the first event followed by direct DNA damage and for the highest concentration a time‐dependent increase in oxidative DNA damage. On BEAS‐2B cells DNA damage was induced within 1 h at 0.5–10 μm , without changes with time, showing that BEAS‐2B cells are able to resist to Cr(VI) genotoxicity. Early oxidative DNA damage at 0.1 μm decreasing with time was also found. Significant apoptosis was observed by morphological analysis in A549 cells and to a lower extent in BEAS‐2B at 10 μm . The exposure to 10 μm induced caspase‐3 activity after 4 h in BEAS‐2B and after 24 h in A549 cells. The findings show a higher responsiveness of A549 cells to genotoxic effect of Cr(VI) and early transient oxidative DNA damage in BEAS‐2B. The results emphasize the suitability of this experimental model to evaluate the early genotoxic response of different cells to non‐cytotoxic concentrations of Cr(VI) on target organ. Copyright © 2009 John Wiley & Sons, Ltd.     

Combination of withaferin A and X-ray irradiation enhances apoptosis in U937 cells

Combined treatment with radiation has improved the outcome in various cancers and many radiosensitizers are used to enhance the therapeutic efficiency of radiotherapy. Withaferin A (Wit A), a natural compound derived from the medicinal plant Withania somnifera, has been reported for its anti-inflammatory and anti-tumor effects. In this study, we show that Wit A enhances the ionizing radiation (IR)-induced apoptosis in human lymphoma U937 cells. Wit A-enhanced IR-induced apoptosis is associated with the PARP cleavage, caspase-3 activation, as well as specifically down-regulation of anti-apoptotic protein Bcl-2, suggesting that Wit A may be useful as a potential radiosensitizer. In addition, pretreatment of U937 cells with SP600125 (JNK inhibitor) or SB203589 (p38 MAPK inhibitor) dose-dependently inhibited the proteolytic cleavage of PARP. We provide the evidence here that generation of reactive oxygen species (ROS), Bcl-2 down-regulation and activation of MAPKs pathway are critically involved in the apoptosis induced by Wit A and radiation.     

瑞舒伐他汀对人胶质瘤U251细胞增殖和凋亡的影响

目的探讨瑞舒伐他汀对人神经胶质瘤U251细胞增殖和凋亡的影响。方法体外培养人神经胶质细胞瘤U251细胞,分别采用5、10、20μmol/L瑞舒伐他汀进行干预,培养24、48、72、96 h,采用MTT比色法检测细胞增殖活性,流式细胞仪检测U251细胞周期的变化。结果处理96 h后,570 nm处吸光度(A570 nm)值变化最明显,瑞舒伐他汀每个浓度组A570 nm值与对照组比较均显著下降(P0.01)。瑞舒伐他汀处理细胞48 h后,与对照组比较,G0/G1期细胞增多,S期和G2/M期细胞减少,且瑞舒伐他汀浓度越大,该作用越强。使用不同浓度瑞舒伐他汀处理48~72 h能诱导U25l细胞凋亡。随着瑞舒伐他汀浓度的增加、作用时间的延长,凋亡峰更加明显,并呈浓度–效应和浓度–时间相关性。结论瑞舒伐他汀对胶质瘤U251细胞增殖具有一定的抑制作用,可以诱导胶质瘤U251细胞凋亡。     

Cytotoxic activity of flavonoids from the flowers of Chrysanthemum morifolium on human colon cancer Colon205 cells

A new p-hydroxyphenylacetyl flavonoid, diosmetin 7-(6″-O-p-hydroxyphenylacetyl)-O-β-d-glucopyranoside (1), was isolated from the flowers of Chrysanthemum morifolium Ramat. ‘huaiju’ cv. nov. (Compositae), together with five known flavonoids, luteolin (2), diosmetin (3), diosmetin 7-O-β-d-glucopyranoside (4), diosmin (5), and scolimoside (6), and four known caffeoylquinic acid derivatives, macranthoin F (7), 3,5-dicaffeoylquinic acid (8), 1,3-dicaffeoyl-epi-quinic acid (9), and chlorogenic acid (10). The structure of 1 was elucidated by UV, IR, ESI-TOF-MS, 1D, and 2D NMR spectroscopic methods. Cytotoxic activity of compounds 1–5 against human colon cancer cell Colon205 was investigated using MTT assays. Compounds 2 and 3 showed significant cytotoxicities against Colon205, with their IC₅₀ values being 96.9 and 82.9 μM, respectively. However, compounds 1, 4, and 5 showed little cytotoxic activity.     

小叶锦鸡儿总黄酮提取工艺研究及对脑缺血再灌注损伤大鼠的作用

目的优化小叶锦鸡儿黄酮类成分的提取工艺,探讨其对实验性脑缺血再灌注损伤大鼠的保护作用。方法采用正交试验,以芦丁作为对照,以总黄酮量为指标考察小叶锦鸡儿总黄酮的最佳提取工艺;采用大脑中动脉阻断（MCAO）制备大鼠局灶性脑缺血再灌注模型,ig给药4周后,观察小叶锦鸡儿总黄酮对MCAO模型大鼠学习记忆能力的影响,并测定其血流变学各项指标。结果正交实验结果表明,各因素作用影响主次顺序为：液固比〉乙醇浓度〉浸提时间〉浸提温度。小叶锦鸡儿总黄酮能提高MCAO模型大鼠的学习记忆能力,降低血浆黏度（η）、血小板聚集率（PAgT）、红细胞聚集指数（EAI）、红细胞刚性指数（IR）,并增加红细胞变形指数（DI）。结论确定了总黄酮最佳提取工艺为乙醇浓度60%,浸提时间5h,液固比40：1,浸提温度60℃。小叶锦鸡儿总黄酮对脑缺血再灌注损伤具有脑保护作用,这可能与小叶锦鸡儿总黄酮降低血黏度有关。     

Induction of cell cycle-dependent cytotoxicity and apoptosis by new heterodinucleoside phosphate dimers of 5-fluorodeoxyuridine in PC-3 human prostate cancer cells

Fluorodeoxyuridine (5-FdUrd) is an antineoplastic agent with clinical activity against different types of solid tumours. To enhance the effectiveness of this drug, we have synthesised new heterodinucleoside phosphate dimers of 5-FdUrd. These dimers were compared to 5-FdUrd for their cytotoxic effect and the cell cycle dependence of cytotoxicity, as well as for their capacity to induce apoptosis and inhibit thymidylate synthetase (TS) in androgen-independent human PC-3 prostate tumour cells. Incubation of the cells with the dimers N(4)-palmitoyl-2'-deoxycytidylyl-(3'-->5')-5-fluoro-2'-deoxyuri din e (dCpam-5-FdUrd) and 2'-deoxy-5-flourouridylyl-(3'-->5')-2'-deoxy-5-fluoro-N(4)-octa decylc ytidine (5-FdUrd-5-FdC18) resulted in a marked cytotoxicity with IC(50) values of 4 microM, similar to 5-FdUrd. In contrast to 5-FdUrd, 100% toxicity was achieved with concentrations of 100-200 microM 5-FdUrd-5-FdC18. Flow cytometric analysis revealed an increase in the cell population in S-phase after treatment with 5-FdUrd, 5-FdUrd-5-FdC18, and dCpam-5-FdUrd from 36 to 63%, 50%, and 77%, respectively. dCpam-5-FdUrd was more potent than 5-FdUrd in arresting the cell cycle. Significant S-phase arrest was indicated by a decreased proportion of cells in G1- and G2/M-phases. Cell cycle arrest and inhibition of cell proliferation were followed by apoptosis, as shown by a 6- to 8-fold increased binding of Apo2.7 antibody, a 9- to 11-fold increase in caspase-3 activity, DNA fragmentation, and by cell morphology showing the appearance of apoptotic bodies. Importantly, 5-FdUrd-5-FdC18 increased the number of apoptotic cells to 160% compared to 5-FdUrd under the same conditions. As with 5-FdUrd, the two dimers also inhibited TS in a time- and concentration-dependent manner, although requiring 100-fold higher concentrations. In conclusion, dCpam-5-FdUrd and 5-FdUrd-5-FdC18 exert stronger cytotoxicity and induce more S-phase arrest and apoptosis than does 5-FdUrd in PC-3 cells, suggesting their potential role in the treatment of human prostate cancer.     

Induction of apoptosis by esculetin in human leukemia U937 cells through activation of JNK and ERK

Esculetin is a phenolic compound that is found in various natural plant products and induces apoptosis in several types of human cancer cells. However, the underlying mechanisms of its action are not completely understood. In the present study, we used human leukemia cells to gain further insight into the mechanism of esculetin-induced anti-proliferative action and apoptosis. It was found that esculetin inhibits cell viability by inducing apoptosis, as evidenced by the formation of apoptotic bodies, DNA fragmentation, and the accumulation of cells in the sub-G1 phase. Esculetin-induced apoptosis was correlated with mitochondrial dysfunction, leading to the release of cytochrome c from the mitochondria to the cytosol, as well as the proteolytic activation of caspases. The z-DEVD-fmk caspase-3 inhibitor and the ectopic expression of anti-apoptotic Bcl-2 significantly inhibited esculetin-induced apoptosis, demonstrating the important role of caspase-3 and mitochondrial proteins in the observed cytotoxic effect. Furthermore, esculetin selectively increased the phosphorylation of extracellular-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK), but not that of other kinases such as Akt and p38 activation. In addition, an ERK-specific inhibitor, PD98059, and a JNK-specific inhibitor, SP600125, showed inhibited sub-G1 phase DNA content, DNA fragmentation, caspase activation, and mitochondrial dysfunction induced by esculetin treatment. These results indicated that the JNK and ERK pathways were key regulators of apoptosis in response to esculetin in human leukemia U937 cells.     

Beta-sitosterol induces anti-proliferation and apoptosis in human leukemic U937 cells through activation of caspase-3 and induction of Bax/Bcl-2 ratio

Beta-sitosterol is the main dietary phytosterol found in plants and has been shown to inhibit proliferation and induce apoptosis in human solid tumors such as colon and breast cancers. However, the mechanism by which beta-sitosterol induces apoptosis is not completely understood in leukemic cells. This study investigated the mechanism of apoptosis induced by beta-sitosterol in human leukemic U937 cells. beta-Sitosterol induced cytotoxicity and apoptosis in U937 cells in a concentration dependent manner, as measured by hemocytometer counts, fluorescence microscopy, agarose gel electrophoresis, and flow cytometry analysis. The increase in apoptosis induced by beta-sitosterol was associated with down-regulation of Bcl-2, degradation of poly-(ADP-ribose) polymerase (PARP) and phospholipase C (PLC)-gamma1 protein, and activation of caspase-3. beta-Sitosterol induced apoptosis was not associated with changes in the expression of Bcl-xL, Bax, or inhibitor of apoptosis proteins (IAPs). z-DEVD-fmk, a caspase-3 specific inhibitor, blocked caspase-3 activation and PARP degradation, and significantly attenuated beta-sitosterol-induced apoptosis. This suggests that caspase-3 activation is partially essential for beta-sitosterol-induced apoptosis. Bcl-2 overexpression also significantly blocked caspase-3 activation and the decrease in PARP cleavage by beta-sitosterol, and effectively attenuated the apoptotic response to beta-sitosterol. These results show that beta-sitosterol potently induces apoptosis in U937 cells and that beta-sitosterol-induced apoptosis is related to the selective activation of caspase-3 and induction of Bax/Bcl-2 ratio.     

Involvement of intrinsic mitochondrial pathway in neosergeolide-induced apoptosis of human HL-60 leukemia cells: The role of mitochondrial permeability transition pore and DNA damage

Context: Quassinoids are biologically active secondary metabolites found exclusively in the Simaroubaceae family of plants. These compounds generally present important biological properties, including cytotoxic and antitumor properties.

Objective: In the present study, the cytotoxic effects of neosergeolide, a quassinoid isolated from Picrolemma sprucei Hook. f., were evaluated in human promyelocytic leukemia cells (HL-60).

Materials and methods: Cytotoxicity and antiproliferative effects were evaluated by the MTT assay, May-Grünwald-Giemsa’s staining, BrdU incorporation test, and flow cytometry procedures. The comet assay and micronuclei analysis were applied to determine the genotoxic and mutagenic potential of neosergeolide.

Results: After 24?h exposure, neosergeolide strongly inhibited cancer cell proliferation (IC₅₀ 0.1 µM), and its activity seemed to be selective to tumor cells because it had no antiproliferative effect on human peripheral blood mononuclear cells (PBMC) at tested concentrations. Apoptosis was induced at submicromolar concentrations (0.05, 0.1, and 0.2 µM) as evidenced by morphological changes, mitochondrial depolarization, phosphatidylserine externalization, caspases activation, and internucleosomal DNA fragmentation. Additionally, neosergeolide effects were prevented by cyclosporine A (CsA), an inhibitor of the mitochondrial permeability transition (MPT) pore, which reinforced the participation of intrinsic pathways in the apoptotic process induced by this natural quassinoid. Direct DNA damage was further confirmed by comet assay and cytokinesis-block micronucleus test.

Discussion and conclusion: The present study provided experimental evidence to support the underlying mechanism of action involved in the neosergeolide-mediated apoptosis. In addition, no antiproliferative effect or DNA damage effect of neosergeolide was evident in PBMC, highlighting its therapeutic potential.     

Kalopanaxsaponin A induces apoptosis in human leukemia U937 cells through extracellular Ca influx and caspase-8 dependent pathways

In the present study, we investigated the effect of KPS-A on the apoptotic activity and the molecular mechanism of the action in human leukemia. Treatment with KPS-A significantly increased apoptotic DNA fragmentation in human histiocytic lymphoma U937 cells as shown by DAPI staining, flow cytometry, and agarose gel electrophoresis. In addition, stimulation of U937 cell with KPS-A induced a series of intracellular events: (1) the activations of caspase-8, caspase-9, and caspase-3; (2) the translocations of Bid and Bax proteins to mitochondria; (3) the loss of mitochondrial membrane potential; and (4) the increased release of cytochrome c to the cytosol. Pretreatment with a specific caspases-8, -9 or -3 inhibitor, neutralized the pro-apoptotic activity of KPS-A in U937 cells. We further demonstrated that KPS-A markedly induced an increase in intracellular Ca²⁺ level, which was reversed by EGTA, a general calcium chelator, but not by TMB-8 and dantrolene, intracellular Ca²⁺ release blockers. Moreover, KPS-A-induced DNA fragmentation and caspase activation were substantially reduced in the presence of EGTA. Taken together, these results suggest that KPS-A may play therapeutic role for leukemia via the potent apoptotic activity through Ca²⁺/caspases-8/MPT/caspases-9/caspases-3 signaling pathway.     

Isolation of eugenyl β-primeveroside from Camellia sasanqua and its anticancer activity in PC3 prostate cancer cells

Most studies of tea trees have focused on their ornamental properties, there are fewer published studies on their medical values. The purpose of this study was to compare the chemical constituents and the biological potential of the water extract of leaves in eight species of Camellia including Camellia sinensis. Among eight Camellia species, Camellia sasanqua showed potent anticancer activities in prostate cancer PC3 cells. In addition to catechins, the major component, eugenyl β-primeveroside was detected in C. sasanqua. Eugenyl β-primeveroside blocked the progression of cell cycle at G1 phase by inducing p53 expression and further upregulating p21 expression. Moreover, eugenyl β-primeveroside induced apoptosis in PC3 prostate cancer cells. Our results suggest that C. sasanqua may have anticancer potential.     

Terminoside A,a new triterpene glycoside from the bark of Terminalia arjuna inhibits nitric oxide production in murine macrophages

Terminoside A (1), a new oleanane-type triterpene was isolated from the acetone fraction of the ethanolic extract of stem bark of Terminalia arjuna. The structure was established as olean-1α,3β,22β-triol-12-en-28-oic acid-3β-D-glucopyranoside. On the basis of spectral data and chemical reactions, terminoside A, potently inhibited nitric oxide (NO) production and decreased inducible nitric oxide synthase (iNOS) levels in lipopolysaccharide-stimulated macrophages.