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Diallyl sulfide (DAS), diallyl disulfide (DADS) and diallyl trisulfide (DATS) are most common components of garlic, and exhibit anticancer activity. However, the exact molecular mechanism of those compounds action with regard to the drug resistance in cancer cells is unclear. Therefore, the purpose of this study was to determine whether DAS, DADS and DATS affected ERK, JNK expression which are associated with the expression of NF-κB that were associated with drug resistance in human colon cancer colo 205 cells in vitro. The methods for those experiments include flow cytometric analysis, Western blotting and PCR. The human colon cancer colo 205 cells treated with or without various concentrations of DAS, DADS and DATS for various time periods then isolating the cells to determine the percentage of viable cells indicated that those compounds decrease viable cell numbers. Western blotting examinations demonstrated that DAS, DADS and DATS decreased the levels of protein kinase c, PI3K and Ras but DAS and DATS inhibited Erk levels and DADS did not affect Erk levels. Furthermore, only DAS promoted JNK levels in colo 205 cells. Three compounds all inhibited VEGF levels which are associated with angigenosis. We also found out that 3 examined compounds affected COX-2 and NF-κB in culture colo 205 cells for 48 hours treatment. Those results also were confirmed by PCR which demonstrated that those compounds affect mRNA gene expression in examined cells. As a whole, our results show that there is a decrease of MDR and Mrp levels in colo 205 after treated with various concentrations of DAS, DADS and DATS. [ABSTRACT FROM AUTHOR]

In this study, MJ-29(6-pyrrolidinyl-2-(2-substituted phenyl)-4-quinazolinones derivatives) was examined for its growth inhibition effect on U937 human leukemia cell line. After 24 hours treatment of MJ-29,PI incorporation was applied to determine the proliferation rate. A dose and time-dependent decrease in cell proliferation was observed. The cytotoxic effect of MJ-29 on normal cells (HUVEC and peripheral mononuclear cells) was lower than that on U937 cells of treatment. Cell cycle analysis of U937 cells showed that MJ-29 induced significant G2/M arrest and apoptosis. Immuno-fluorescence microscopy and in vitro tubulin assembly assays indicated that MJ-29 binding to tubulin and disrupts microtubule organization. We found that MJ-29 up-regulated the protein levels of p161-CDK1,Chk1,Chk2,p21 and increased cyclin B and CDK1 kinase activity. MJ-29-treated U937 cells presented typical apoptosis by DAPI staining, increase of Annexin V binding, internucleosomal DNA cleavage. In addition, release of cytosolic cytochrome c¡BPro-caspase-9¡BApaf-1 and AIF, down-regulation of Bcl-2, Bcl-xL¡B xIAP¡BclAP-1¡BclAP-2 and up-regulation of phospho-Bcl-2¡BBax¡BBad¡BBak were detected by western blotting. Caspases activity assay and Sub-G1 nuclei analysis of MJ-29-treated U937 indicated that the MJ-29 induced apoptosis was mainly mediated by activation of caspase 9 and 3. Our results indicated that the ability of MJ-29 to inhibit cell proliferation may be mediated by both the induction of mitotic arrest and apoptosis. µ [ABSTRACT FROM AUTHOR]

Rutin, one of the flavonoids, possesses a wide range of biological effects, including antitumor, antioxidant, and anti-inflammatory activities and anti-leukeima cells. Although rutin had been reported to induce apoptosis via caspase-3 activation on human leukemia K562 cells, there is no available information to address whether or not rutin affects leukemia cells in vivo. However, the exact effect of rutin on leukemia cells on murine in vivo is undefined. Therefore, in the present we are focused on the effects of rutin in vivo affecting WEHI-3 cells on murine leukemia. These experiments were divided into 3 parts. Part 1, we examined the effects of rutin on the percentage of viable cells by flow cytometry on WEHI-3 cells in vitro and the results indicated that rutin decreased the viable cells and those effects are dose-and time-dependent effect manners. Part II, we examined the effects of rutin on leukemia WEHI-3 cells in BLAB/c mice in vivo and the results indicated that rutin decreased the percentage of Mac-3 marker, inhibiting the differentiation of precursor of macrophage and T cells which were isolated from spleen. Part III, we examined the size and weight changes of liver and spleen and the results demonstrated that rutin decreased the size and weight of liver and spleen when comparing to the control group. One of the characters of leukemia is the enlarged spleen in murine after i.p. was injected with WEHI-3 cells. Part IV, in the pathological examination, rutin affected the liver and spleen which came from the BLAB/c mice i.p. after injected with WEHI-3 cells treated with or without rutin. Our result showed that rutin affects WEHI-3 cells in vitro and in vivo. [ABSTRACT FROM AUTHOR]

Evidence has accumulated that berberine induced cell cycle arrest and apoptosis in many human cancer cell lines. However, there is no available information to address berberine affecting human oral quamous carcinoma cancer HSC-3 cells. In this study, we have examined the effects of berberine on cell growth and apoptosis and cell cycle regulation in human oral squamous carcinoma HSC-3 cells. Berberine induced dose- and time-dependent of irreversible inhibition of cell growth and cellular DNA synthesis. It was also confirmed by phase-light microscopy which showed that berberine induced morphological changes in HSC-3 cells. Propidium iodide/annexin V staining for flow cytometric analysis showed that berberine induced apoptosis correlating with caspase-3 activation in examined cells. Flow cytometry studies of the cell cycle distribution showed that berberine induced mainly G0/G1-phase arrest. Flow cytometry examinations also showed that berberine induced reactive oxygen species (ROS) and Ca2+ production and dysfunction of mitochondrial membrane potential (MMP) which are correlated with apoptosis. In conclusion, our data supports a view that berberine initially induces an endoplasmic reticulum stress response based on ROS and Ca2+ production then followed by dysfunction mitochondria, resulting in apoptosis of these oral cancer HSC-3 cells. Prolonged exposure of the HSC-3 cells to berberine causes increased percentage of apoptosis through decreased levels of MMP, cytochrome c release and activation of caspase-3. [ABSTRACT FROM AUTHOR]

Dietary polyphenols have been demonstrated to reduce risk of chronic diseases such as cancer, but the precise underlying mechanism of protection remains unclear. Quercetin, one of the flavonoids found in onion, grapes, green vegetables, etc., possesses a wide range of biological effects including potent antiproliferative effects against various malignant cells. However, the exact effect of leukemia cells on murine in vivo is undefined. The aim of this study was to investigate the effect of quercetin on affecting murine leukemia WEHI-3 cells in vivo. The cytotoxicity analysis demonstrated that quercetin inhibited the growth of WEHI-3 cells in dose- and time- dependent manners. After animals were injected with i.p by WEHI-3 cells that were oral treated with quercetin, the animals were sacrificed to measure the body weight and the results demonstrated that quercetin decreased both the size and weight of liver and spleen. Based on the ELISA analysis, it was demonstrated that quercetin decreased the percentage of Mac-3 marker and it also inhibited the differentiation of precursor of macrophage and T cells. Based on the pathological examination after animals were injected with i.p. through WEHI-3 with or without orally treated quercetin, it was demonstrated that quercetin did affect spleen and liver tissues. Therefore, the function of quercetin was observed in the liver and spleen of mice previously injected with WEHI-3 cells. The results from flow cytometric analysis also demonstrated that quercetin promoted the killing target cells of natural killer cells from mouse. Apparently, our results demonstrated that quercetin affects WEHI-3 cells in vitro and in vivo. [ABSTRACT FROM AUTHOR]

Wogonin is one of the flavonoids and it has been shown to exert antioxidant, anti-viral, anti-bacteria, anti-thrombotic, anti-inflammatory and cytostatic activities. Recently, it also has been reported that wogonin induced apoptosis of human leukemia cells. Importantly, wogonin lacks toxicity for normal peripheral blood mononuclear cells. However, there is no available information to address whether or not wogonin affects leukemia cells in vivo. In this study, we investigated the effects of wogonin in vivo affecting murine leukemia WEHI-3 cells. This study is divided into in vitro and in vivo, the in vitro studies, it indicated that wogonin inhibit cell proliferation of WEHI-3 using MTT assay and those effects are dose-and time-dependent manners. The in vivo studies, the major assay is flow cytometry and the results indicated 1) wogonin inhibit the percentage of Mac-3 marker, inhibiting the differentiation of precursor of macrophage and T cells; 2) wogonin decrease the weights of liver and spleen after comparying to non-treated groups; 3) wogonin decreased the sizes of liver and spleen. The results indicated that wogonin affects WEHI-3 cells in vitro and in vivo. Wogonin may be used for therapy of leukemia. [ABSTRACT FROM AUTHOR]