Guangdong Provincial Institute of Sports Science

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Guangdong Provincial Institute of Sports Science

Science, China
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Song A.,Chongqing University | Song A.,Guangdong Provincial Institute of Sports Science | Liao Q.,Chongqing University | Li J.,Purdue University | And 5 more authors.
Toxicology Letters | Year: 2012

Sulfur dioxide (SO2) is a common air pollutant that triggers asthmatic symptoms, but its toxicological mechanisms are not fully understood. Specifically, it is unclear how airborne SO2 affects airway hyperresponsiveness (AHR) - a hallmark feature of asthma. To this end, we investigated the effects of chronic exposure to SO2 on AHR, airway inflammation, tissue remodeling, cell stiffness (G') and contractility of the airway smooth muscle cell (ASMC). Newborn Sprague-Dawley (SD) rats sensitized to ovalbumin (OVA) was used as the model to mimic asthmatic symptoms. The experimental results show that exposure to SO2: (1) significantly increased Penh (an indicator of AHR) in the OVA-sensitized rats (p<0.01) but not in the normal rats (p>0.05), which correlated with the increase of airway smooth muscle mass; (2) increased IL-4 production in BALF of both the normal (p<0.05) and OVA-sensitized rats (p<0.001), but decreased IFN-γ in BALF of only the normal rats, and in serum only increased IL-4 production of the OVA-sensitized rats (p<0.001); (3) increased ASMC stiffness (G') and contractility only in the OVA-sensitized rats (p<0.001, p<0.05, respectively). Taken together, these results demonstrate that SO2 may be a universal airway inflammatory factor, but more importantly, specific to exacerbating AHR in asthmatics only. These findings uncover a potential mechanism of SO2-induced health effects and may provide a basis for therapeutic targets. © 2012.


Song A.-J.,Guangdong Provincial Institute of Sports Science | Deng J.-J.,Guangdong Provincial Institute of Sports Science | Lv X.-H.,Guangdong Provincial Institute of Sports Science | Zhang Y.,Guangdong Provincial Institute of Sports Science
Chinese Journal of Tissue Engineering Research | Year: 2015

BACKGROUND: Isokinetic test has been generally used as an objective indicator for assessing the functional state and sports injury of the muscle system in athletes. OBJECTIVE: To explore the isokinetic muscle strength characteristics of the knee, ankle and trunk in football players. METHODS: Cybex-Norm isokinetic testing system was used to test the flexion and extension peak torque, relative peak torque and relative endurance of the isokinetic double knees double ankles and trunk at different angular velocity. RESULTS AND CONCLUSION: There was no significant difference between the muscle strength of the bilateral knees and ankles (< 5%). The extensor peak torque and relative peak torque of the knee were lower, and the flexor peak torque and relative peak torque of the knee were higher, especially in the left knee, which is not conductive to the effective completion of ball control, kicking and vertical jump. The relative peak torque of the trunk was relatively weak, which is prone to damage during exercise and results lower back pain. Relative endurances of the knee, ankle and trunk are not satisfied, which can be improved greatly. © 2015, Journal of Clinical Rehabilitative Tissue Engineering Research. All rights reserved.


Li Z.,Shanghai University of Sport | Li Z.,Guangdong Provincial Institute of Sports Science | Hong P.,China Institute of Sport Science | Wu Y.,Shanghai University of Sport | And 2 more authors.
Chinese Journal of Tissue Engineering Research | Year: 2016

BACKGROUND: Due to the differences of sport events and individual metabolic characteristics of athletes, it is difficult to establish uniform biological indexes for training monitoring. Current individual evaluation is a longitudinal analysis relying on experience or numerical variation width, which is less objective. OBJECTIVE: To explore the individual function assessment and monitoring by monitoring blood biochemical indexes and brain function indexes in elite gymnasts, in order to accurately reflect the body changes resulting from training loads. METHODS: Thirty gymnasts from the Chinese national gymnastics team preparing for London Olympic Games were enrolled in this study and monitored from the last winter training until the London Olympic Games. The blood biochemical indicators and brain function indicators were measured and assessed individually according to according to the principle of quality control (alert value=mean±SD, and controlled variable=mean±2SD). RESULTS AND CONCLUSION: Under the relatively uniform test conditions, it is feasible to individually assess the blood biochemical and brain function indexes of elite gymnasts in accordance with the principle of quality control, which is more accurate and objective to reflect the body changes under training load and the current state of athletes. In addition, the combined monitoring of blood biochemical indexes and brain function indexes is more comprehensive to evaluate the body function and status of elite gymnasts. © 2016, Journal of Clinical Rehabilitative Tissue Engineering Research. All rights reserved.


Zhou J.-J.,Sun Yat Sen University | Deng X.-G.,Sun Yat Sen University | He X.-Y.,Guangdong Provincial Institute of Sports Science | Zhou Y.,Sun Yat Sen University | And 6 more authors.
International Journal of Oncology | Year: 2014

Multidrug resistance (MDR) is one of the major reasons for the failure of liver cancer chemotherapy, and its suppression may increase the efficacy of chemotherapy. NANOG plays a key role in the regulation of embryonic stem cell self-renewal and pluripotency. Recent studies reported that NANOG was abnormally expressed in several types of tumors, indicating that NANOG is related to tumor development. However, the correlation between NANOG and liver cancer chemoresistance remains uncertain. In this study, RNA interfere technology was employed to knock down NANOG expression in HepG2 human liver cancer cells. We found that the knockdown of NANOG expression in NANOG siRNA-transfected HepG2 cells resulted in decreased colony formation rate and cell migration compared to control HepG2 cells. In addition, HepG2 cells were treated with doxorubicin to evaluate the chemosensitivity to doxorubicin. We found that the doxorubicin sensitivity of HepG2 cells was increased with downregulation of NANOG expression. The expression of MDR1 at both mRNA and protein levels was decreased in HepG2 cells when NANOG was knocked down. These findings suggest that the knockdown of NANOG in HepG2 human cells resulted in decreased MDR1 expression and increased doxorubicin sensitivity, and NANOG could be used as a novel potential therapeutic target to reverse multidrug resistance of liver cancer.


Zhou J.-J.,Sun Yat Sen University | Chen R.-F.,Sun Yat Sen University | Deng X.-G.,Sun Yat Sen University | Zhou Y.,Sun Yat Sen University | And 8 more authors.
FEBS Letters | Year: 2014

HCV Core plays a role in the development of hepatocellular carcinoma. Aberrant expression of NANOG has been observed in many types of human malignancies. However, relationship between Core and NANOG has not been clarified. In this study, we found that Core is capable of up-regulating NANOG expression. Core-induced NANOG expression was accompanied by enforced expression of phosphorylated stat3 protein and was attenuated by inhibition of stat3 phosphorylation. ChIP showed that phosphorylated stat3 directly binds to the NANOG promoter. Core-induced NANOG expression resulted in enhanced cell growth and cell cycle progression. Knockdown of NANOG blocked the cell cycle at the G0/G1 phases and inhibited the cyclin D1 expression. Our findings provide a new insight into the mechanism of hepatocarcinogenesis by HCV infection. © 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.


Song A.,Changzhou University | Song A.,Guangdong Provincial Institute of Sports Science | Lin F.,Changzhou University | Li J.,Purdue University | And 4 more authors.
Inhalation Toxicology | Year: 2014

Sulfur dioxide (SO2) is a common air pollutant that triggers asthmatic symptoms, but its toxicological mechanisms are not fully understood. Specifically, it is unclear how SO2 in vivo affects airway smooth muscle (ASM) cells of which the mechanics is known to ultimately mediate airway hyperresponsiveness (AHR)-a hallmark feature of asthma. To this end, we investigated the effects of bisulfite/sulfite (1:3 M/M in neutral fluid to simulate the in vivo derivatives of inhaled SO2 in the airways), on the viability, migration, stiffness and contractility of ASM cells cultured in vitro. The results showed that bisulfite/sulfite consistently increased viability, migration, F-actin intensity and stiffness of ASM cells in similar fashion as concentration increasing from 10-4 to 10 -1mmol/L. However, bisulfite/sulfite increased the ASM cell contractility induced by KCl only at the concentration between 10-4 and 10-3mmol/L (p<0.05), while having no consistent effect on that induced by histamine. At the concentration of 100mmol/L, bisulfite/sulfite became acutely toxic to the ASM cells. Taken together, the data suggest that SO2 derivatives at low levels in vivo may directly increase the mass, stiffness and contractility of ASM cells, which may help understand the mechanism in which specific air pollutants contribute in vivo to the pathogenesis of asthma. © 2014 Informa Healthcare USA, Inc.


Lin F.,Chongqing University | Song A.,Guangdong Provincial Institute of Sports Science | Wu J.,Chongqing University | Jiang X.,Chongqing University | And 6 more authors.
Molecular Medicine Reports | Year: 2013

A disintegrin and metalloproteinase 33 (ADAM33) has been identified as an asthma susceptibility gene; however, the role of ADAM33 in the pathogenesis and progression of asthma remains to be elucidated. As ADAM33 is predominantly expressed in airway smooth muscle cells (ASMCs), it is feasible to investigate whether ADAM33 protein expression is correlated with ASMC mechanics that are ultimately responsible for airway hyperresponsiveness in asthma. To determine this, Sprague Dawley rats were sensitized with ovalbumin (OVA) for up to 12 weeks to simulate asthma symptoms. Subsequently, ASMCs were isolated from the rats and cultured in vitro. The protein expression of ADAM33 and cytoskeletal proteins (including F-actin and vinculin), cell stiffness and contractility, as well as traction force were measured. The results demonstrated that compared with the non-sensitized rats, the protein expression of ADAM33 in ASMCs from the OVA-sensitized rats increased in a time-dependent manner, reaching a maximum level at 4 weeks of sensitization and gradually subsiding as OVA sensitization continued (P<0.001). The cell stiffness, traction force and expression of vinculin and F-actin changed similarly, resulting in a positive correlation with ADAM33 protein expression (Pearson's correlation coefficient, 0.864, 0.716, 0.774 and 0.662, respectively; P=0.1-0.3). The in vivo results of OVA-induced ADAM33 protein expression and its association with the mechanics of ASMCs suggested that ADAM33 is a mediator of ASMC dysfunction in asthma, and may provide a rationale for the therapeutic targeting of ADAM33 in the treatment of asthma.


Liu K.-P.,Jinan University | Zhou D.,Jinan University | Ouyang D.-Y.,Jinan University | Xu L.-H.,Jinan University | And 4 more authors.
Biochemical and Biophysical Research Communications | Year: 2013

Autophagy is a conserved mechanism for controlling the degradation of misfolded proteins and damaged organelles in eukaryotes and can be induced by nutrient withdrawal, including serum starvation. Although differential acetylation of autophagy-related proteins has been reported to be involved in autophagic flux, the regulation of acetylated microtubule-associated protein 1 light chain 3 (LC3) is incompletely understood. In this study, we found that the acetylation levels of phosphotidylethanolamine (PE)-conjugated LC3B (LC3B-II), which is a critical component of double-membrane autophagosome, were profoundly decreased in HeLa cells upon autophagy induction by serum starvation. Pretreatment with lysosomal inhibitor chloroquine did not attenuate such deacetylation. Under normal culture medium, we observed increased levels of acetylated LC3B-II in cells treated with tubacin, a specific inhibitor of histone deacetylase 6 (HDAC6). However, tubacin only partially suppressed serum-starvation-induced LC3B-II deacetylation, suggesting that HDAC6 is not the only deacetylase acting on LC3B-II during serum-starvation-induced autophagy. Interestingly, tubacin-induced increase in LC3B-II acetylation was associated with p62/SQSTM1 accumulation upon serum starvation. HDAC6 knockdown did not influence autophagosome formation but resulted in impaired degradation of p62/SQSTM1 during serum starvation. Collectively, our data indicated that LC3B-II deacetylation, which was partly mediated by HDAC6, is involved in autophagic degradation during serum starvation. © 2013 Elsevier Inc.


Wang L.,Jinan University | Wang L.,Guangdong Provincial Institute of Sports Science | Li C.,Jinan University | Lin Q.,Jinan University | And 6 more authors.
Acta Biochimica et Biophysica Sinica | Year: 2015

Cucurbitacin E (CucE), a triterpenoid isolated from Cucurbitaceae plants, has been shown to possess an anti-inflammatory or immunosuppressive activity in vitro and in vivo, yet the underlying mechanism has been incompletely understood. The aim of the present study was to explore its effect on cytokine expression and the underlying mechanism in human Jurkat T cells as a cellular model. The results showed that CucE significantly inhibited the production of interleukin-2, tumor necrosis factor- α, and interferon-γ in culture medium of cells treated with phorbol 12,13-dibutyrate (PDB) plus ionomycin (Ion). Furthermore, the mRNA levels of these cytokines in activated Jurkat T cells were also decreased upon CucE treatment, suggesting a potential modulatory effect on the critical signaling pathways for cytokine expression, including nuclear factor-κB (NF-κB) or mitogen-activated protein kinases (MAPKs). In support of its effect on the NF-κB signaling pathway, CucE decreased the phosphorylation levels of inhibitor of κB (IκB) and NF-κB/p65 in PDB + Ion-stimulated cells. Further supporting this, the nuclear translocation of NF-κB/p65 was significantly suppressed in response to PDB plus Ion stimulation in the presence of CucE. The phosphorylation of p38MAPK, c-Jun N-terminal kinase (JNK), and Erk1/2, however, was not decreased or slightly increased at some time points by CucE treatment. Collectively, these data suggest that CucE may exhibit immunosuppressive effect by attenuating critical cytokine expression through down-regulating the NF-κB signaling pathway. © The Author 2015.

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