Zhang Y.,Guangdong Pharmaceutical University
African journal of traditional, complementary, and alternative medicines : AJTCAM / African Networks on Ethnomedicines | Year: 2013
Juglans mandshurica Maxim is a traditional herbal medicines in China, and its anti-tumor bioactivities are of research interest. Bioassay-guided fractionation method was employed to isolate anti-tumor compounds from the stem barks of the Juglans mandshurica Maxim. The anti-tumor effect and biological activities of the extracted compound JMM6 were studied in BEL-7402 cells by MTT, Cell cycle analysis, Hoechst 33342 staining, Annexin V-FITC/PI assay and Detection of mitochondrial membrane potential (ΔΨm). After treatment with the JMM6, the growth of BEL-7402 cells was inhibited and cells displayed typical morphological apoptotic characteristics. Further investigations revealed that treatment with JMM6 mainly caused G2/M cell cycle arrest and induced apoptosis in BEL-7402 cells. To evaluate the alteration of mitochondria in JMM6 induced apoptosis. The data showed that JMM6 decreased significantly the ΔΨm, causing the depolarization of the mitochondrial membrane. Our results show that the JMM6 will have a potential advantage of anti-tumor, less harmful to normal cells. This paper not only summarized the JMM6 pick-up technology from Juglans mandshurica Maxim and biological characteristic, but also may provide further evidence to exploit the potential medicine compounds from the stem-barks of the Chinese Juglans mandshurica Maxim.
Wang S.,South China University of Technology |
Wang S.,Guangdong Pharmaceutical University |
Zhou S.,South China University of Technology
Journal of Hazardous Materials | Year: 2011
A novel nanoscale photocatalyst CNTs/P-TiO2 was successfully prepared by hydrothermal method. The morphology and the physicochemical properties of the prepared samples were investigated using TEM, XPS, XRD, BET, FTIR, TG-DSC and UV-vis DRS spectroscopy. The photocatalytic activity was evaluated by degradation of methyl orange (MO) dye. The results demonstrated that CNTs/P-TiO2 nanoparticles could effectively photodegrade MO not only under UV irradiation but also under visible-light (VL) irradiation. The MO degradation performance on CNTs/P-TiO2 was superior to that of the commercial P25. The optimal mass ratio of CNTs to P-TiO2 in the nanocomposite catalyst was 5:100. The synergetic effect was discussed in terms of different roles played by phosphorus doping and introducing CNTs into the composite catalysts. © 2010.
Zhang Q.-X.,Guangdong Pharmaceutical University
Oncogene | Year: 2016
Aberrant p62 overexpression has been implicated in breast cancer development. Here, we found that p62 expression was elevated in breast cancer stem cells (BCSCs), including CD44+CD24- fractions, mammospheres, ALDH1+ populations and side population cells. Indeed, short-hairpin RNA (shRNA)-mediated knockdown of p62 impaired breast cancer cells from self-renewing under anchorage-independent conditions, whereas ectopic overexpression of p62 enhanced the self-renewal ability of breast cancer cells in vitro. Genetic depletion of p62 robustly inhibited tumor-initiating frequencies, as well as growth rates of BCSC-derived tumor xenografts in immunodeficient mice. Consistently, immunohistochemical analysis of clinical breast tumor tissues showed that high p62 expression levels were linked to poorer clinical outcome. Further gene expression profiling analysis revealed that p62 was positively correlated with MYC expression level, which mediated the function of p62 in promoting breast cancer stem-like properties. MYC mRNA level was reduced upon p62 deletion by siRNA and increased with p62 overexpression in breast cancer cells, suggesting that p62 positively regulated MYC mRNA. Interestingly, p62 did not transactivate MYC promoter. Instead, p62 delayed the degradation of MYC mRNA by repressing the expression of let-7a and let-7b, thus promoting MYC mRNA stabilization at the post-transcriptional level. Consistently, let-7a and let-7b mimics attenuated p62-mediated MYC mRNA stabilization. Together, these findings unveiled a previously unappreciated role of p62 in the regulation of BCSCs, assigning p62 as a promising therapeutic target for breast cancer treatments.Oncogene advance online publication, 27 June 2016; doi:10.1038/onc.2016.202. © 2016 Macmillan Publishers Limited
Chu F.J.,Guangdong Pharmaceutical University
Journal of atherosclerosis and thrombosis | Year: 2011
To investigate the effects of housefly maggot (Musca domestica) protein-enriched fraction/extracts (PE) on lipopolysaccharide (LPS)-induced atherosclerosis (AS) pro-inflammatory responses in mice and macrophages. The mouse model of AS was established by feeding a cholesterol-enriched diet and inducing by LPS. Changes in the levels of blood lipids (total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL) and high-density lipoprotein cholesterol (HDL)) and pro-inflammatory cytokines (interferon-gamma (IFNγ), tumor necrosis factor alpha (TNFα) and interleukin-1alpha (IL-1α)) were determined. Histomorphometric analysis of the pathological condition of the artery was also carried out. The macrophages were stimulated by LPS in the presence or absence of PE, and then the levels of TNFα, IL-1α and monocyte chemotactic protein 1 (MCP-1) in cell culture supernatant were measured. Compared with the negative control group, the levels of three pro-inflammatory cytokines were significantly enhanced in the PE treatment group (p< 0.01). The concentrations of TC, TG and LDL were lower in the PE treatment group than in the negative control group (p< 0.01). HDL concentration in the PE treatment group was higher than in the negative control group (p< 0.01). Histomorphometric analysis showed that the thickness of the intima and media area, as well as the area ratio of the intima to media in the PE treatment group were lower than in the negative control group (p< 0.01). The expression of TNFα, IL-1α and MCP-1 in LPS-induced macrophages was inhibited by different concentrations of PE (p< 0.01). These results indicate that PE potently inhibited multiple pro-inflammatory responses in experimental atherosclerosis lesions in vivo, and possessed anti-pro-inflammatory properties in vitro.
Pan X.,Guangdong Pharmaceutical University
Nan fang yi ke da xue xue bao = Journal of Southern Medical University | Year: 2013
To study the effect of apigenin on the proliferation and apoptosis of human lung cancer cell line NCI-H460. NCI-H460 cells were cultured with different concentrations of apigenin, and MTT assay was used to evaluate the cell inhibition rates. Apoptosis of NCI-H460 cells was observed under a fluorescence microscope with Hoechst 33258 staining and quantified by flow cytometry using annexin V-FITC/PI stain. The expressions of apoptosis-related proteins Bax, Bcl-2 and caspase-3 were analyzed by Western blotting. Apigenin causes concentration- and time-dependent inhibition of the proliferation of the cells. NCI-H460 cells treated with apigenin showed significant morphological changes of apoptosis, and the cell apoptotic rates increased as apigenin concentration increased. Western blotting demonstrated that apigenin increased the protein levels of Bax and caspase-3 and reduced the protein expression of Bcl-2. Apigenin can inhibit the proliferation and induce apoptosis of NCI-H460 cells possibly by up-regulating expression of Bax and caspase-3 and down-regulating the expression of Bcl-2.