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Articles by Z Hou
Total Records ( 2 ) for Z Hou
  T Zou , W Yang , Z Hou and J. Yang
 

Elevation of blood homocysteine levels (hyperhomocysteinemia) is a risk factor for cardiovascular disorders. One of the mechanisms by which homocysteine induces atherosclerosis is to promote the proliferation of vascular smooth muscle cells (VSMCs) in a reactive oxygen species (ROS)-dependent manner. It has been shown that homocysteine induces the production of ROS through the activation of NAD(P)H oxidases in VSMCs. In this study, we investigated the signal transduction pathways involved in the activation of NAD(P)H oxidases. Homocysteine promoted DNA synthesis in VSMCs. Inhibition of ROS by N-acetyl-l-cysteine (an antioxidant) and apocynin (an inhibitor of NAD(P)H oxidases) significantly blocked homocysteine-induced proliferation in VSMCs. Homocysteine induced a rapid increase in the phosphorylation of p38-mitogen-activated protein kinase (p38 MAPK). p38 MAPK in turn activated NAD(P)H oxidases by inducing the phosphorylation of p47phox, resulting in the generation of ROS. ROS induced the phosphorylation of Akt, which was probably responsible for proliferation in VSMCs. These findings demonstrate that homocysteine induces an increase in the activity of NAD(P)H oxidases in VSMCs by activating p38 MAPK and enhancing the phosphorylation of p47phox.

  G. X Li , Y. K Chen , Z Hou , H Xiao , H Jin , G Lu , M. J Lee , B Liu , F Guan , Z Yang , A Yu and C. S. Yang
 

(–)-Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, has been shown to inhibit tumorigenesis and cancer cell growth in animal models. Nevertheless, the dose–response relationship of the inhibitory activity in vivo has not been systematically characterized. The present studies were conducted to address these issues, as well as the involvement of reactive oxygen species (ROS), in the inhibitory action of EGCG in vivo and in vitro. We characterized the inhibitory actions of EGCG against human lung cancer H1299 cells in culture and in xenograft tumors. The growth of tumors was dose dependently inhibited by EGCG at doses of 0.1, 0.3 and 0.5% in the diet. Tumor cell apoptosis and oxidative DNA damage, assessed by the formation of 8-hydroxy-2'-deoxyguanosine (8-OHdG) and phosphorylated histone 2A variant X (-H2AX), were dose dependently increased by EGCG treatment. However, the levels of 8-OHdG and -H2AX were not changed by the EGCG treatment in host organs. In culture, the growth of viable H1299 cells was dose dependently reduced by EGCG; the estimated concentration that causes 50% inhibition (IC50) (20 µM) was much higher than the IC50 (0.15 µM) observed in vivo. The action of EGCG was mostly abolished by the presence of superoxide dismutase (SOD) and catalase, which decompose the ROS formed in the culture medium. Treatment with EGCG also caused the generation of intracellular ROS and mitochondrial ROS. Although EGCG is generally considered to be an antioxidant, the present study demonstrates the pro-oxidative activities of EGCG in vivo and in vitro in the described experimental system.

 
 
 
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