Guangdong Pharmaceutical University

www.gdpu.edu.cn
Guangzhou, China

Guangdong Pharmaceutical University is a public university based in Guangzhou, Guangdong Province, China, which offers courses in pharmaceutical science. Wikipedia.

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Patent
Guangdong Pharmaceutical University | Date: 2015-12-30

The present invention discloses a preparation and application of flavonol as a brain-targeting synergist. After long-term repeated studies, the inventors have found that some flavonol compounds, particularly kaempferide, rutin, troxerutin, myricetin, hesperidin, and hydroxy derivatives thereof, in particular their glycoside, ester, ether derivatives, can promote the drug molecules that have therapeutic or healthcare effect, such as ginsenoside, stilbene glucoside, resveratrol, levodopa, edaravone, vinpocetine, nicergoline, citicoline, oxiracetam, to enter brain tissues, to dramatically enhance drugs concentrations in the brain tissues and effective enhance the efficacy of drugs without increasing the plasma concentration.


Patent
Guangdong Pharmaceutical University | Date: 2017-03-08

The present invention discloses an application of ruthenium complexes as nucleic acid vectors of target cell nucleuses. Experimental data shows that ruthenium (II) complexes may be effectively combined with nucleic acid sequence and may effectively change morphologies of long sequence nucleic acids to make the nucleic acids be effectively delivered into viable cells via transmembrane transport and be well located within cell nucleuses, thus greatly improving transport efficiency of the nucleic acids. Based on this property, nucleic acid sequences can be conveniently transported into cells for gene therapy or fluorescent tracking or the like. The method for preparing a ruthenium coordination complex-nucleic acid complex in accordance with the present invention may provide a stable ruthenium coordination complex-nucleic acid complex in a more efficient manner and may provide many better effects.


Patent
Guangdong Pharmaceutical University | Date: 2016-03-03

The present invention discloses an application of ruthenium complexes as nucleic acid vectors into target cell nucleuses. Experimental data shows that ruthenium (II) complexes may be effectively combined with nucleic acid sequence and may effectively change morphologies of long nucleic acid sequences to effectively deliver the nucleic acids into viable cells via transmembrane transport located within cell nucleuses, thus greatly improving transport efficiency of the nucleic acids. Based on this property, nucleic acid sequences can be conveniently transported into cells for gene therapy or fluorescent tracking or the like. The method for preparing a ruthenium coordination complex-nucleic acid complex in accordance with the present invention may provide a more effective and stable ruthenium coordination complex-nucleic acid complex.


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


Pan H.,Guangdong Pharmaceutical University | Guo J.,Guangdong Pharmaceutical University | Su Z.,Guangdong Pharmaceutical University
Physiology and Behavior | Year: 2014

Obesity, which has developed into a global epidemic, is a risk factor in most chronic diseases and some forms of malignancy. The discovery of leptin in 1994 has opened a new field in obesity research. Currently, we know that leptin is the primary signal from energy stores and exerts negative feedback effects on energy intake. However, most individuals with diet-induced obesity (DIO) develop leptin resistance, which is characterized by elevated circulating leptin levels and decreased leptin sensitivity. To date, though various mechanisms have been proposed to explain leptin resistance, the exact mechanisms of leptin resistance in obesity are poorly understood. Consequently, it's an important issue worth discussing regarding what the exact interrelations between leptin resistance and obesity are. Here, we review the latest advancements in the molecular mechanisms of leptin resistance and the exact interrelations between leptin resistance, obesity, and obesity-related diseases, in order to supply new ideas for the study of obesity. © 2014 Elsevier Inc.


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.


Patent
Guangdong Pharmaceutical University | Date: 2016-06-17

The present invention relates to a method for the preparation of Medicated Leaven Massa by pure strain fermentation, characterized in that the Medicated Leaven Massa is prepared by fermentation under suitable conditions with Penicillium chrysogenum as a single fermentative strain and the culture medium is made of 6 ingredients, including flour (and/or wheat bran), Artemisia carvifolia, Polygonum flaccidum Meissn., Xanthium sibiricum Patr., Semen Armeniacae Amarum., and Vigna umbellata.


The present invention relates to a composition of extracts from plants which can be used for prophylaxis or treatment of metabolism disorder of blood lipid, which belongs to the pharmaceutical technology. The plant extract composition provided by the present invention includes the following ingredients in weight: 3-10 portions of oleanolic acid, 1-5 portions of salvianolic acid, 1-5 portions of danshensu, 1-3 portions of berberine, 1-5 portions of panax notoginseng saponins, 1-5 portions of polysaccharides of atracty-lodes macrocephala koidz, 1-3 portions of aucubin, 1-5 portions of total flavone in cirsium japonicum, 1-5 portions of fmger citron polysaccharide, 1-5 portions of panax notoginseng polysaccharides and 1-5 portions of flavones. The present invention also provides the use of such composition in manufacturing medicaments used for prophylaxis or treatment of diseases related to metabolism disorder of blood lipid, and the use of such composition in manufacturing health food used for adjuvant prophylaxis or treatment of diseases related to metabolism disorder of blood lipid. The plant extract composition provided by the present invention has broadened the application of the existing technology in the field of pharmaceutical preparations, which significantly improves the bioavailability, increase the effectiveness, stability, controllability, convenience and safety of medication.

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