Higher Education Mega Center

Panyu District, China

Higher Education Mega Center

Panyu District, China
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Yang Y.,Higher Education Mega Center | Wang W.,Higher Education Mega Center | Xiong Z.,Higher Education Mega Center | Kong J.,Higher Education Mega Center | And 5 more authors.
Pharmazie | Year: 2016

Clinical application of triptolide (TP), a main active ingredient of the traditional Chinese herb Tripterygium wilfordii Hook f. (TWHF), is limited by a series of severe toxicities, including cardiotoxicity. In previous studies, we found the activation of sirtuin 3 (SIRT3) attenuated TP-induced toxicity in cardiomyocytes. Resveratrol (RSV), a polyphenol from the skins of grapes and red wine, is an activator of SIRT3. The current study aimed to investigate the protective effect of RSV against TP-induced cardiotoxicity and the underlying mechanisms. Mice were treated with a single dose of TP (2.5 mg/kg) via the intragastric (i.g.) route. After 24 h, TP induced abnormal changes of serum biochemistry, activity decrease of antioxidant enzymes and damage of heart tissue such as myocardial fiber rupture, cell swelling and interstitial congestion. In contrast, administration with RSV (50 mg/kg i.g. 12 h before and 2 h after the administration of TP) attenuated the detrimental effects induced by TP in BALB/c mice. Moreover, the cardiomyocyte protective effects of RSV on TP-induced heart injury were associated with the activation of SIRT3 and its downstream targets. In vitro study also indicated that RSV counteracted TP-induced cardiotoxicity through SIRT3-FOXO3 signaling pathway in H9c2 cells. Collectively, these findings suggest the potential of RSV as a promising agent in protecting heart from TP-induced damage. © 2016, Govi-Verlag Pharmazeutischer Verlag GmbH. All rights reserved.


Luo T.,Sun Yat Sen University | Wang G.,Higher Education Mega Center | Wang G.,Sun Yat Sen University
Optical Engineering | Year: 2016

This work provides a design and optimization method for total internal reflection (TIR) lenses based on slope-error tolerance analysis. This work focuses on how the slope error impacts the central luminous intensity (CLI) of a TIR lens. The concentration standard index (CSI) is introduced as a metric for analyzing the CLI, both locally and globally. A unique design method for improved manufacturing tolerance is introduced, and a way of optimizing the TIR lens design in order to achieve a better slope-error tolerance is presented by evaluating the CSI. Using the design method, a TIR lens is fabricated and this theoretical approach is then demonstrated by a comparison between the tested contours of the TIR surfaces. © 2016 The Authors.


Kang Y.,Higher Education Mega Center | Kang Y.,Hong Kong Baptist University | Man Y.B.,Hong Kong Baptist University | Cheung K.C.,Hong Kong Baptist University | And 2 more authors.
Environmental Science and Technology | Year: 2012

There is limited information on the bioaccessible fractions of phthalate esters in indoor dust in order to estimate human exposure. In the present study, workplace dust and settled house dust samples from Hong Kong, Shenzhen, and Guangzhou, the three major cities scattered around the Pearl River Delta (PRD) were collected. Chemical analyses showed that the phthalates in workplace dust ranged from 144 to 1810 μg/g, with dust from shopping malls containing the highest level, and in home dust ranged from 181 to 9240 μg/g. The most abundant phthalate ester found was bis(2-ethylhexyl) phthalate (DEHP) in both workplace dust and home dust, followed by di-n-butyl phthalate (DBP) and di-iso-butyl phthalate (DIBP). Principal Components Analysis (PCA) indicated that indoor dust around PRD showed similar phthalate esters patterns of composition. A significant correlation was observed between total phthalate esters concentrations in home dust and the number of year of house construction (p < 0.05). The oral bioaccessibility of phthalate esters in indoor dust ranged from 10.2% (DEHP) to 32% (DMP). Risk assessment indicated that the dominant exposure routes varied in different phthalate esters exposure profiles and the dermal contact exposure pathway was identified as an important route for indoor DEHP exposure. © 2012 American Chemical Society.


Chen Y.,Guangzhou University | Tang Q.,Guangzhou University | Wu J.,Guangzhou University | Zheng F.,Guangzhou University | And 3 more authors.
Journal of Experimental and Clinical Cancer Research | Year: 2015

Background: Lung cancer is the most common cause of cancer-related deaths worldwide. Natural phytochemicals from traditional medicinal plants such as solamargine have been shown to have anticancer properties. The prostaglandin E2 receptor EP4 is highly expressed in human cancer, however, the functional role of EP4 in the occurrence and progression of non small cell lung cancer (NSCLC) remained to be elucidated. Methods: Cell viability was measured by MTT assays. Western blot was performed to measure the phosphorylation and protein expression of PI3-K downstream effector Akt, transcription factors SP1, p65, and EP4. Quantitative real-time PCR (qRT-PCR) was used to examine the mRNA levels of EP4 gene. Exogenous expression of SP1, p65, and EP4 genes was carried out by transient transfection assays. EP4 promoter activity was measured by Dual Luciferase Reporter Kit. Results: We showed that solamargine inhibited the growth of lung cancer cells. Mechanistically, we found that solamargine decreased the phosphorylation of Akt, the protein, mRNA expression, and promoter activity of EP4. Moreover, solamargine inhibited protein expression of SP1 and NF-κB subunit p65, all of which were abrogated in cells transfected with exogenous expressed Akt. Intriguingly, exogenous expressed SP1 overcame the effect of solamargine on inhibition of p65 protein expression, and EP4 protein expression and promoter activity. Finally, exogenous expressed EP4 feedback reversed the effect of solamargine on phosphorylation of Akt and cell growth inhibition. Conclusion: Our results show that solamargine inhibits the growth of human lung cancer cells through inactivation of Akt signaling, followed by reduction of SP1 and p65 protein expression. This results in the inhibition of EP4 gene expression. The cross-talk between SP1 and p65, and the positive feedback regulatory loop of PI3-K/Akt signaling by EP4 contribute to the overall responses of solamargine in this process. This study unveils a novel mechanism by which solamargine inhibits growth of human lung cancer cells. © 2015 Chen et al.


Yang L.,Guangzhou University | Tang Q.,Guangzhou University | Wu J.,Guangzhou University | Chen Y.,Guangzhou University | And 4 more authors.
Journal of Experimental and Clinical Cancer Research | Year: 2016

Background: Ursolic acid (UA), a natural pentacyclic triterpenoid, exerts anti-tumor effects in various cancer types including hepatocellular carcinoma (HCC). However, the molecular mechanisms underlying this remain largely unknown. Methods: Cell viability and cell cycle were examined by MTT and Flow cytometry assays. Western blot analysis was performed to measure the phosphorylation and protein expression of p38 MAPK, insulin-like growth factor (IGF) binding protein 1 (IGFBP1) and forkhead box O3A (FOXO3a). Quantitative real-time PCR (qRT-PCR) was used to examine the mRNA levels of IGFBP1 gene. Small interfering RNAs (siRNAs) method was used to knockdown IGFBP1 gene. Exogenous expressions of IGFBP1 and FOXO3a were carried out by transient transfection assays. IGFBP1 promoter activity was measured by Secrete-Pair™ Dual Luminescence Assay Kit. In vivo nude mice xenograft model and bioluminescent imaging system were used to confirm the findings in vitro. Results: We showed that UA stimulated phosphorylation of p38 MAPK. In addition, UA increased the protein, mRNA levels, and promoter activity of IGFBP1, which was abrogated by the specific inhibitor of p38 MAPK (SB203580). Intriguingly, we showed that UA increased the expression of FOXO3a and that overexpressed FOXO3a enhanced phosphorylation of p38 MAPK, all of which were not observed in cells silencing of endogenous IGFBP1 gene. Moreover, exogenous expressed IGFBP1 strengthened UA-induced phosphorylation of p38 MAPK and FOXO3a protein expression, and more importantly, restored the effect of UA-inhibited growth in cells silencing of endogenous IGFBP1 gene. Consistent with these, UA suppressed tumor growth and increased phosphorylation of p38 MAPK, protein expressions of IGFBP1 and FOXO3a in vivo. Conclusion: Collectively, our results show that UA inhibits growth of HCC cells through p38 MAPK-mediated induction of IGFBP1 and FOXO3a expression. The interactions between IGFBP1 and FOXO3a, and feedback regulatory loop of p38 MAPK by IGFBP1 and FOXO3a resulting in reciprocal pathways, contribute to the overall effects of UA. This in vitro and in vivo study corroborates a potential novel mechanism by which UA controls HCC growth and implies that the rational targeting IGFBP1 and FOXO3a can be potential for the therapeutic strategy against HCC. © 2016 Yang et al.


Wu J.,Guangzhou University | Zhao S.,Guangzhou University | Tang Q.,Guangzhou University | Zheng F.,Guangzhou University | And 7 more authors.
Journal of Experimental and Clinical Cancer Research | Year: 2015

Background: Ursolic acid (UA), a pentacyclic triterpenoid, is known to have anti-tumor activity in various cancers including human non small cell lung cancer (NSCLC). However, the molecular mechanisms underlying the action of UA remain largely unknown. Methods: Cell viability was measured by MTT assays. Apoptosis was analyzed with Annexin V-FITC/PI Apoptosis Detection Kit by Flow cytometry. Western blot analysis was performed to measure the phosphorylation and protein expression of stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK), DNMT1 [DNA (cytosine-5)-methyltransferase 1], enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) and SP1. Exogenous expression of SP1 and DNMT1 was carried out by transient transfection assays. Results: We showed that UA inhibited the growth and induced apoptosis of NSCLC cells in the dose- and time-dependent fashion. Furthermore, we found that UA induced phosphorylation of SAPK/JNK and suppressed the protein expression of DNMT1 and EZH2. The inhibitor of SAPK/JNK (SP600125) blocked the UA-reduced expression of DNMT1 and EZH2. In addition, UA suppressed the expression of SP1 protein. Conversely, overexpression of SP1 reversed the effect of UA on DNMT1 and EZH2 expression, and feedback attenuated UA-induced phosphorylation of SAPK/JNK. Moreover, exogenous expression of DNMT1 antagonized the effect of UA on SAPK/JNK signaling, EZH2 protein expression, and NSCLC cell growth. Conclusion: Our results show that UA inhibits growth of NSCLC cells through SAPK/JNK-mediated inhibition of SP1; this in turn results in inhibition the expression of DNMT1 and EZH2. Overexpression of DNMT1 diminishes UA-reduced EZH2 protein expression. The negative feedback regulation of SAPK/JNK signaling by SP1 and DNMT1, and the reciprocal interaction of EZH2 and DNMT1 contribute to the overall effects of UA. This study leads to important new insights into the mechanisms by which UA controls growth of NSCLC cells. © 2015 Wu et al.


Zheng F.,Guangzhou University | Wu J.,Guangzhou University | Li X.,Guangzhou University | Tang Q.,Guangzhou University | And 6 more authors.
Evidence-based Complementary and Alternative Medicine | Year: 2016

The aim of this study is to investigate the actions of Chinese herbal medicine, called "Fuzheng Kang-Ai" (FZKA for short) decoction, against non-small cell lung cancer (NSCLC) and its mechanisms in vitro and in vivo. We showed that the effect of FZKA decoction significantly inhibited growth of A549 and PC9 cells. Furthermore, FZKA increased phosphorylation of AMP-activated protein kinase alpha (AMPKα) and induced protein expression of insulin-like growth factor (IGF) binding protein 1 (IGFBP1) and forkhead homeobox type O3a (FOXO3a). The specific inhibitor of AMPKα (Compound C) blocked FZKA-induced protein expression of IGFBP1 and FOXO3a. Interestingly, silencing of IGFBP1 and FOXO3a overcame the inhibitory effect of FZKA on cell growth. Moreover, silencing of IGFBP1 attenuated the effect of FZKA decoction on FOXO3a expression, and exogenous expression of FOXO3a enhanced the FZKA-stimulated phosphorylation of AMPKα. Accordingly, FZKA inhibited the tumor growth in xenograft nude mice model. Collectively, our results show that FZKA decoction inhibits proliferation of NSCLC cells through activation of AMPKα, followed by induction of IGFBP1 and FOXO3a proteins. Exogenous expression of FOXO3a feedback enhances FZKA decoction-stimulated IGFBP1 expression and phosphorylation of AMPKα. The reciprocal interplay of IGFBP1 and FOXO3a contribute to the overall responses of FAKA decoction. © 2016 Fang Zheng et al.


Juan Y.,Higher Education Mega Center | Xuesong H.,Higher Education Mega Center
International Journal of Applied Environmental Sciences | Year: 2013

This paper presents QoS routing protocol (QBR) of wireless Mesh network based on environmental bandwidth cognition. It takes available environment bandwidth as the main routing criterion, comprehensively considering various factors on business characteristics, priority level of user, available environment bandwidth of network and so on, introduces thought like preemption compression etc, can make full use of network resources, avoid unnecessary routing reconstruction, realize the network equilibrium, reduce the risk of refusing to accept.The simulation results show that the protocol algorithm of QBR routing has higher ratio of data delivery and more obvious advantages on improving the transmission quality of the network etc. © Research India Publications.

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