Jianguang L.,Xingtai Medical College |
Jinyuan Z.,Hebei Civil Administration General Hospital |
Jundong H.,Xingtai University |
Bin Z.,Xingtai University |
And 10 more authors.
BioTechnology: An Indian Journal | Year: 2013
Objective: To understand the research hotspots of Hepatitis virology by PubMed. Methods: With MS Excel, SPSS, Cytoscape software, we took MeSH (Medical Subject Headings) word frequency analysis, clustering analysis, co-word network graph of PubMed papers. Results: It shows that the currentHepatitis virology research hotspots had focus onHepatitis C and B,AntiviralAgents, etc, also the most importance of which was the HepatitisC.Conclusion: It is helpful and timesaving for researcher or doctor to understand the research hotspots in Hepatitis virology. © 2013 Trade Science Inc. - INDIA.
Zhou J.,Zhejiang University |
Xu X.-Z.,Liver Disease Branch |
Hu Y.-R.,Liver Disease Branch |
Hu A.-R.,Liver Disease Branch |
Zhu C.-L.,Wuhan University
Asian Pacific Journal of Cancer Prevention | Year: 2014
Cryptotanshinone (CPT), is a quinoid diterpene isolated from the root of the Asian medicinal plant, Salvia miotiorrhiza bunge. Numerous researchers have found that it could work as a potent antitumor agent to inhibit tumor growth in vitro, buith there has been much less emphasis on its in vivo role against breast tumors. Using a mouse tumor model of MCF7 cells, we showed that CPT strongly inhibited MCF7 cell growth in vivo with polarization of immune reactions toward Th1-type responses, stimulation of naive CD4+ T cell proliferation, and also increased IFN-γ and perforin production of CD4+ T cells in response to tumor-activated splenocytes. Furthermore, data revealed that the cytotoxic activity of CD4+ T cells induced by CPT was markedly abrogated by concanamycin A(CMA), a perforin inhibitor, but not IFN-γ Ab. On the other hand, after depletion of CD4+ T cells or blocked perforin with CMA in a tumor-bearing model, CPT could not effectively suppress tumor growth, but this phenomenon could be reversed by injecting naive CD4+ T cells. Thus, our results suggested that CPT mainly inhibited breast tumor growth through inducing cytotoxic CD4+ T cells to secrete perforin. We further found that CPT enhanced perforin production of CD4+ T cells by up-regulating JAK2 and STAT4 phosphorylation. These findings suggest a novel potential therapeutic role for CPT in tumor therapy, and demonstrate that CPT performs its antitumor functions through cytotoxic CD4+ T cells.