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Jing-Tian Xie,Guang-Jian Du,Eryn McEntee,Han H. Aung,Hui He,Sangeeta R. Mehendale,Chong-Zhi Wang,Chun-Su Yuan 대한암학회 2011 Cancer Research and Treatment Vol.43 No.1
Purpose The pharmacological activities, notably the anticancer properties, of bioactive constituents from fresh American ginseng berry have not yet been well studied. In this study, we investigated the antiproliferative effects of fresh American ginseng berry extract (AGBE) and its representative triterpenoid glycosides using the human colorectal cancer cell line SW480. Materials and Methods Using high performance liquid chromatography (HPLC), the contents of 8 ginsenosides in AGBE were determined. The cell growth inhibitory effects of AGBE and three triterpenoid glycosides (ginsenosides Rb3, Re, and Rg3) were evaluated by proliferation assay and 3H-thymidine incorporation assay. Cell cycle and apoptotic effects were analyzed by using flow cytometry after staining with propidium iodide and annexin V. Results HPLC analysis data showed that AGBE has a distinct ginsenoside profile. AGBE inhibited SW480 cell growth significantly in a time-dependent (24-96 hours) and concentration-dependent (0.1-1.0 mg/mL) manner. Ginsenosides Rb3, Re, and Rg3 also possess significant antiproliferative activities on SW480 cells. 3H-thymidine incorporation assay indicated that AGBE and ginsenosides Rb3, Re, and Rg3 might inhibit the transferring and duplication of DNA in SW480 cells. Flow cytometric assay data suggested that AGBE arrested SW480 cells in S and G2/M phases, and significantly induced cell apoptosis. Conclusion AGBE and ginsenosides Rb3, Re, and Rg3 possessed significant antiproliferative effects and induced changes of morphological appearance on SW480 cells. The mechanisms of the antiproliferation of AGBE and tested ginsenosides involved could be cell cycle arrest and induction of apoptosis.
Xiao-dong Yao,Zheng-Chun Du,Guang-yan Ge,Jian-Guo Yang 대한기계학회 2020 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.34 No.1
In this work, a novel machine tool thermal error modeling method based on dynamic temperature gradient is proposed, and a thermal error compensation method based on unfalsified control is developed. The dynamic temperature gradient is used to optimize the locations of temperature measuring points on the machine tool. Real-time compensation for the thermal error can be achieved using the developed compensation method by establishing the correlations between dynamic temperature gradient and thermal error in the machine tool. Different from traditional model-based methods, the developed compensation approach does not rely on an accurate model of the thermal error but instead uses online input/output data to adaptively select the best controller at any moment, thereby improving thermal error prediction accuracy and robustness. The effectiveness of the developed thermal error compensation method is demonstrated on a turning center, where the spindle thermal error is compensated during the manufacturing of 120 inner bore parts and 120 shaft parts. After compensation using the proposed approach, thermal errors are reduced from 27 µm to 9 µm for the inner bore parts and from 31 µm to 11 µm for the shaft parts, respectively.
Three New 11,20-Epoxy-ent-kauranoids from Isodon rubescens
Xu Liu,Ji Zhou Wu,Rui Zhan,Wei Guang Wang,Xue Du,Yan Li,Peng Zhang,Jian Xin Pu,Han Dong Sun 대한약학회 2012 Archives of Pharmacal Research Vol.35 No.12
Three rare and new 11,20-epoxy-ent-kaurane diterpenoids, named jianshirubesins D-F (1-3), along with one known analogue (4), were isolated from the aerial parts of Isodon rubescens. Their structures were established by analysis of spectroscopic data. Found in the MTT assay to evaluate the cytotoxicity of compounds 1, 2, and 4, only 1 could selectively inhibit certain cell lines from proliferating. In addition, a simple structure-activity relationship discussion might suggest a new bioactive moiety, different from the α,β-unsaturated ketone group.
Li, Chen-Long,Chang, Liang,Guo, Lin,Zhao, Dan,Liu, Hui-Bin,Wang, Qiu-Shi,Zhang, Ping,Du, Wen-Zhong,Liu, Xing,Zhang, Hai-Tao,Liu, Yang,Zhang, Yao,Xie, Jing-Hong,Ming, Jian-Guang,Cui, Yu-Qiong,Sun, Ying Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.23
Background: ${\beta}$-elemene, extracted from herb medicine Curcuma wenyujin has potent anti-tumor effects in various cancer cell lines. However, the activity of ${\beta}$-elemene against glioma cells remains unclear. In the present study, we assessed effects of ${\beta}$-elemene on human glioma cells and explored the underlying mechanism. Materials and Methods: Human glioma U87 cells were used. Cell proliferation was determined with MTT assay and colony formation assay to detect the effect of ${\beta}$-elemene at different doses and times. Fluorescence microscopy was used to observe cell apoptosis with Hoechst 33258 staining and change of glioma apoptosis and cell cycling were analyzed by flow cytometry. Real-time quantitative PCR and Western-blotting assay were performed to investigated the influence of ${\beta}$-elemene on expression levels of Fas/FasL, caspase-3, Bcl-2 and Bax. The experiment was divided into two groups: the blank control group and ${\beta}$-elemne treatment group. Results: With increase in the concentration of ${\beta}$-elemene, cytotoxic effects were enhanced in the glioma cell line and the concentration of inhibited cell viability ($IC_{50}$) was $48.5{\mu}g/mL$ for 24h. ${\beta}$-elemene could induce cell cycle arrest in the G0/G1 phase. With Hoechst 33258 staining, apoptotic nuclear morphological changes were observed. Activation of caspase-3,-8 and -9 was increased and the pro-apoptotic factors Fas/FasL and Bax were upregulated, while the anti-apoptotic Bcl-2 was downregulated after treatment with ${\beta}$-elemene at both mRNA and protein levels. Furthermore, proliferation and colony formation by U87 cells were inhibited by ${\beta}$-elemene in a time and does-dependent manner. Conclusions: Our results indicate that ${\beta}$-elemene inhibits growth and induces apoptosis of human glioma cells in vitro. The induction of apoptosis appears to be related with the upregulation of Fas/FasL and Bax, activation of caspase-3,-8 and -9 and downregulation of Bcl-2, which then trigger major apoptotic cascades.