Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
 
Articles by X Chu
Total Records ( 2 ) for X Chu
  B Li , X Chu , M Gao and W. Li
 

The aim of this study was to investigate the pro-apoptotic mechanism of C-phycocyanin (C-PC)-mediated photodynamic therapy (PDT) in a murine tumor model and cultured MCF-7 cells. The mice were divided into four groups: control, He–Ne laser radiation, C-PC treatment, and C-PC treatment + He–Ne laser radiation. The effects of C-PC and/or laser on immune organs, immunocyte proliferation, tumor genesis, and apoptosis-related proteins expressions were investigated by immunohistochemistry, in situ hybridization, MTT, electron microscope, western blot, and immunofluorescence assay. The results showed that He–Ne laser treatment alone showed marginal effects. In C-PC-treated mice, the weight of immune organs, proliferation of immunocytes, and expression of pro-apoptotic Fas protein were increased, whereas the tumor weight and the expressions of anti-apoptotic proteins (NF-B and P53) and CD44 mRNA were comparatively decreased. In vitro, C-PC was able to inhibit MCF-7 cell proliferation and cause ultrastructural changes including microvilli loss, formation of membrane blebs, and chromatin condensation. Moreover, C-PC treatment could activate caspase-9 expression, induce cytochrome c release, and downregulate Bcl-2 expression. When combined with He–Ne laser irradiation, the effects of C-PC treatment were further enhanced. Facilitating the apoptosis signals transduction and finally leading to the apoptosis of MCF-7 cells may be the mechanism of the anti-tumor activities of C-PC-mediated PDT.

  Y Wang , D Liang , S Wang , Z Qiu , X Chu , S Chen , L Li , X Nie , R Zhang , Z Wang and D. Zhu
 

It has been previously reported by us that hypoxia activates lung 15-lipoxygenase (15-LO), which catalyzes arachidonic acid to 15-hydroxyeicosatetraenoic acid (15-HETE), leading to the constriction of pulmonary artery (PA). Rho-associated serine/threonine kinase (ROK), a downstream effector of small GTPase RhoA that may be modulated by G-protein and tyrosine kinase, plays an important role in smooth muscle contraction. However, whether the 15-HETE induced PA vasoconstriction involves the Rho/ROK pathway remains to be demonstrated. Therefore, we studied the contribution of ROK as well as G-protein and tyrosine kinase to the 15-HETE induced pulmonary vasoconstriction using PA ring technique, RNA interference technology, RP-HPLC, western blot and RT-PCR combined with the blockers. The hypoxia-induced expression of ROK is regulated by 15-HETE in rat PA smooth muscle cells (PASMCs), leading to vasoconstriction. The up-regulation of ROK expression caused by 15-HETE appears to be mediated by the G-protein and tyrosine kinase pathways. The translocation of ROK2 from the nucleus to the cytoplasm during hypoxia exposure relies on the mechanism for 15-HETE production. These results suggest that 15-HETE may mediate the up-regulation of ROK expression through G-protein and tyrosine kinase pathways under hypoxic condition, leading to PA vasoconstriction.

 
 
 
Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility