Qingshan Yang

Central South University, Ch’ang-sha-shih, Hunan, China

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Publications (5)9.67 Total impact

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    ABSTRACT: Advanced glycation end products (AGEs) is an important mediator in Osteoarthritis (OA), and causes apoptosis in articular chondrocytes. Mitochondrial function is involved in modulating apoptosis of articular chondrocytes. The present study was performed to investigate the mechanism of AGEs-induced chondrocyte apoptosis. The ratio of apoptotic cell and cell viability was surveyed by TUNEL, MTT,LDH release assay. The reactive oxygen species was determined by the fluorescent probe 2’, 7’-dichlorofluorescein diacetate. The expression of caspase-3 and cytochrome c was detected by western blot. The mitochondrial membrane potential (△Ψm) was evaluated by Rhodamine-123 fluorescence. We found that AGEs induced apoptosis in primary rabbit chondrocytes, up-regulation of ROS production, cytochrome c and caspase-3 levels. Simultaneously, AGEs decreases the levels of △Ψm and ATP production, however, the antibody of AGEs (sRAGE) and antioxidant-N-acetylcys-teine (NAC), significantly reversed AGEs-induced the above damage thus to protect the cells from apoptosis. These observations suggested that the mechanism of AGEs-induced chondrocyte apoptosis was primarily via ROS production and mitochondria-mediated caspase-3 activation.This article is protected by copyright. All rights reserved.
    No preview · Article · Oct 2014 · Fundamental and Clinical Pharmacology
  • Shujin Wu · Xiang Gao · Shehua Yang · Liying Liu · Bin Ge · Qingshan Yang
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    ABSTRACT: Aims: Recent studies have reported that intracellular calcium (Ca(2+)) mobilization is involved in homocysteine (Hcy)-induced endothelial dysfunction and the Na(+)/H(+) exchanger (NHE) is responsible for an increase in the intracellular Ca(2+) concentration in cardiovascular disease. We hypothesized that inhibition of the NHE had protective effects on Hcy-induced endothelial dysfunction. Methods: Acetylcholine-induced endothelium-dependent relaxation (EDR) and biochemical parameters were measured in the rat isolated aorta. The level of reactive oxygen species (ROS) was designed by a specific fluorescent probe. The phosphorylation of the nuclear factor-κB (NF-κB) system was studied by Western blot. Results: Cariporide significantly prevented Hcy-impaired EDR and increased nitric oxide (NO) release; endothelial NO synthase activity simultaneously decreased ROS production. We also found that cariporide blocked Hcy-induced NF-κB activation and inhibitor-κB degradation, thus inhibiting the production of tumor necrosis factor-α and intercellular adhesion molecule-1. Conclusions: The mechanisms of protective effects of cariporide may be related to the inhibition of NHE and the decrease in oxidative stress and inflammatory injury.
    No preview · Article · Nov 2013 · Pharmacology
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    ABSTRACT: Aims: The association between diabetes and neointimal expansion after vascular injury has been attributed to the accumulation of advanced glycation end products (AGEs). Here we investigated the inhibitory effect of cariporide, a specific Na(+)/H(+) exchanger 1 blocker, on neointimal proliferation induced by AGEs in a balloon injury model. Methods: Expression of cyclooxygenase-2 (COX-2) and matrix metalloproteinase (MMP) was monitored by reverse transcription-polymerase chain reaction (RT-PCR) and real-time PCR. The level of reactive oxygen species (ROS) was determined by specific fluorescent probe. The phosphorylation of the nuclear factor-ĸB (NF-ĸB) system was studied by Western blot. Results: Cariporide significantly suppressed AGE-induced neointimal hyperplasia, vascular smooth muscle cell (VSMC) proliferation, COX-2, MMP-2 and MMP-9 expression. In addition, cariporide decreased AGE-induced ROS, malondiadehyde level and increased the superoxide dismutase and glutathione peroxidase activity. We also found that cariporide blocked AGE-induced NF-ĸB activation and inhibitor-ĸB degradation. Conclusions: The results indicated that cariporide inhibited AGE-induced neointimal formation by suppressing the VSMC proliferation and the up-regulation of COX-2, MMP-2, MMP-9 via inhibiting ROS and NF-ĸB activation.
    No preview · Article · Jan 2013 · Pharmacology
  • Qingshan Yang · Shujin Wu · Xinzhan Mao · Wanchun Wang · Huiping Tai
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    ABSTRACT: Aims: Accumulation of advanced glycation end products (AGEs) plays a pivotal role in the mechanism by which aging contributes to osteoarthritis (OA). In the present study, we examined the effect of curcumin, a pharmacologically safe phytochemical agent, on AGE-induced tumor necrosis factor-α (TNF-α) and matrix metalloproteinase-13 (MMP-13) in rabbit chondrocytes. Methods: Chondrocytes were derived from rabbit articular cartilage by enzymatic digestion. TNF-α and MMP-13 mRNA was monitored by RT-PCR. TNF-α protein was determined using cytokine-specific ELISA. The reactive oxygen species was determined by the fluorescent probe 29,79-dichlorofluorescein diacetate. The phosphorylation and nuclear translocation of the nuclear factor-ĸB (NF-ĸB) system were studied by Western blot and immunofluorescence respectively. Results: Curcumin significantly decreased AGE-stimulated TNF-α and MMP-13 mRNA and suppressed the NF-ĸB activation via inhibition of ĸBα (I-ĸBα) phosphorylation, I-ĸBα degradation and p65 nuclear translocation. Conclusions: These novel pharmacological actions of curcumin on AGE-stimulated chondrocytes provide new suggestions that curcumin has nutritional potential as a naturally occurring anti-inflammatory agent for treating OA.
    No preview · Article · Nov 2012 · Pharmacology
  • Qingshan Yang · Cheng Chen · Shujin Wu · Ying Zhang · Xinzhan Mao · Wanchun Wang
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    ABSTRACT: Accumulation of advanced glycation end products (AGEs) which are known to adversely affect cartilage turnover and mechanical properties, provides a molecular mechanism by which aging contributes to the development of osteoarthritis. The objective of the present study was to investigate the role of peroxisome proliferator-activated receptor γ (PPARγ) in AGEs-mediated chondrocytes damage. In the cultured rabbit chondrocytes, our results show that the PPARγ agonist pioglitazone can concentration-dependently inhibit the AGEs-induced expression of TNF-α and MMP-13. Several studies have shown that activation of PPARγ may interfere with several signaling pathways regulating the proinflammatory genes in vivo and vitro experiments, but little is known regarding their expression and regulation in cartilage. Thus the effect of AGEs on PPARγ expression was next examined. Reverse transcription (RT)-PCR analysis revealed that AGEs treatment of chondrocytes downregulated PPARγ expression in a time- and concentration-dependent manner. AGEs-induced a significant downregulation in PPARγ mRNA at 48 h and the maximum effect was found at 100 μg/ml AGEs. This effect was significantly depressed by the anti-RAGE antibody. Specific inhibitors of the mitogen-activated protein kinases (MAPK) p38 (SB203580) and c-Jun N-terminal kinase (SP600125), but not of extracellular signal-regulated kinase (PD98059), prevented AGEs-induced downregulation of PPARγ expression. In conclusion, AGEs may be responsible for PPARγ downregulation via a mechanism involving activation of the MAPK (p38 and JNK), and this downregulation might play a key role in AGEs-induced production of TNF-α and MMP-13.
    No preview · Article · Dec 2010 · European journal of pharmacology

Publication Stats

31 Citations
9.67 Total Impact Points


  • 2013
    • Central South University
      • Department of Pharmacology
      Ch’ang-sha-shih, Hunan, China
  • 2010-2012
    • The Second Xiangya Hospital of Central South University
      Ch’ang-sha-shih, Hunan, China