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	1. ELUCIDATION OF ANTI-APOPTOTIC MECHANISMS OF TANSHINONE IIA REVEALS THE ROLE OF MIR-34 IN CARDIOMYOCYTE APOPTOSIS
	CHU Xia,LU Huimin,BAI Yunlong,XIAO Jiening,PAN Zhenwei,LUO Xiaobin,ZHANG Yong,SHAN Hongli,LU Yanjie,YANG Baofeng,WANG Zhiguo
	Basic Medicine 28 December 2010
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	Abstract:In this paper，microRNAs (miRNAs) have recently emerged as a central player of gene regulatory network involved in decision of cell fate. Apoptosis, an active process that leads to cell death, has been shown to be controlled by miRNAs. It has also been implicated in a variety of human disease, such as heart disease, and established as a target process for disease therapy. Tanshinone IIA (TIIA), a monomer of phenanthrenequinones used to treat cardiovascular diseases, is known to insert cardioprotective effects in myocardial infarction by targeting apoptosis through enhancing Bcl-2 expression. To explore the potential link between miRNAs and the anti-apoptotic action of TIIA, we studied the possible involvement of miRNAs. We found that expression of all three members of the miR-34 family, miR-34a, miR-34b and miR-34c that have been known to mediate the apoptotic effect of p53, was robustly upregulated after exposure to either the DNA-damaging agent doxorubicin or pro-oxidant H2O2 for 24 hr. This upregulation caused significant apoptotic cell death, as determined by DNA fragmentation, and the effects were reversed by the antisense to these miRNAs. Pretreatment of cells with TIIA prior to incubation with doxorubicin or H2O2 prevented upregulation of miR-34 and reduced apoptosis. We then established BCL2L2, API5 and TCL1, in addition to BCL2, as the novel target genes for miR-34. We further unraveled that repression of these genes by miR-34 accounts for their proapoptotic effect in cardiomyocytes whereas upregulation of these genes by TIIA through downregulating miR-34 is likely the molecular mechanism for its beneficial effect against ischemic myocardial injuries.
	TO cite this article:CHU Xia,LU Huimin,BAI Yunlong, et al. ELUCIDATION OF ANTI-APOPTOTIC MECHANISMS OF TANSHINONE IIA REVEALS THE ROLE OF MIR-34 IN CARDIOMYOCYTE APOPTOSIS[OL].[28 December 2010] http://en.paper.edu.cn/en_releasepaper/content/4401790


	2. Effects of the cultured Cordyceps exopolysaccharide (EPS) on some parameters of mouse immune function in vivo and in vitro1
	Weiyun Zhang,Jinyu Yang,Jiaping Chen,Jing Li,Yi Zheng
	Basic Medicine 14 December 2005
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	Abstract:The Cordyceps fungi (CSG1) were cultured and the exopolysaccharide (EPS) was prepared from the culture supernatant. In vivo experiment, ICR mice were treated with three different doses of EPS for seven days. In vitro study, macrophage, spleen and thymus lymphocytes were incubated in the presence of five different concentrations of EPS. The phagocytosis of peritoneal macrophage was determined by neutral red uptake test and the proliferation abilities of spleen and thymus lymphocyte were studied with MTT method. The results of in vivo study illustrated that the macrophage neutral red uptake ability of mice was significantly enhanced by three different doses of EPS (p<0.001) and spleen lymphocyte’s proliferation was elevated at the dose of 60 mg/kg (p<0.01). However, thymus lymphocyte proliferation did not show significant variation compared with the control mice after seven day’s EPS treatment. In vitro study, EPS not only significantly elevated the phagocytosis of peritoneal macrophage in the concentration of 50 and 100 mg/L (p<0.05), but also significantly increased the proliferation abilities of spleen and thymus lymphocytes in 100 mg/L (p<0.001 and p<0.05, respectively). These results suggest that EPS has an immunomodulatory activity on mouse macrophages and lymphocytes, and this ability might be useful for application to assist treating some diseases such as cancers.
	TO cite this article:Weiyun Zhang,Jinyu Yang,Jiaping Chen, et al. Effects of the cultured Cordyceps exopolysaccharide (EPS) on some parameters of mouse immune function in vivo and in vitro1 [OL].[14 December 2005] http://en.paper.edu.cn/en_releasepaper/content/4362

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