严新老师近年发表的几篇研究文章的摘要
1. Mol Cell Biochem. 2008 Mar;310(1-2):227-34.
External Qi of Yan Xin Qigong induces G2/M arrest and apoptosis of androgen-independent prostate cancer cells by inhibiting Akt and NF-kappa B pathways.
Yan X, Shen H, Jiang H, Zhang C, Hu D, Wang J, Wu X.
Long-term clinical observations and ongoing studies have shown antitumor effects of external Qi of Yan Xin Qigong (YXQG-EQ) that originated from traditional Chinese medicine (TCM). In order to understand the molecular mechanisms underlying the antitumor effects of YXQG-EQ, we investigate the effects of YXQG-EQ on growth and apoptosis in androgen-independent prostate cancer PC3 cells. We found that exposure to YXQG-EQ led to G2/M arrest associated with reduced cyclin B1 expression and apoptosis in PC3 cells. YXQG-EQ treatment inhibited constitutive and epidermal growth factor-induced Akt phosphorylation, basal and TNF-alpha-induced NF-kappaB activation, and downregulated anti-apoptotic Bcl-2 and Bcl-xL expression. In contrast, exposure to YXQG-EQ increased phosphorylation of Akt and Erk1/2 in human umbilical vein endothelial cells (HUVEC), and had no cytotoxic effect on either HUVEC or peripheral blood mononuclear cells (PBMC). These results indicate that YXQG-EQ has profound effects on growth and apoptosis of prostate cancer cells by targeting survival pathways including the Akt and NF-kappa B pathways.
2.Int J Neurosci. 2002 Oct;112(10):1209-27.
XY99-5038 promotes long-term survival of cultured retinal neurons.
Yan X, Fong YT, Wolf D, Shen H, Zaharia M, Wang J, Wolf G, Li F, Lee GD, Cao W.
We have previously reported that XY99-5038, a preparation from a specific formula of Traditional Chinese Medicine, could effectively inhibit hydrogen peroxide-induced retinal cell death. In the present study, we investigated the possibility of XY99-5038 to prolong neuronal survival in a long-term retinal neuronal culture. Basic fibroblast survival factor (bFGF), a potent neurotrophic factor, was employed as comparable agent. Retinas of 0-2 days old Sprague-Dawley rats were isolated and dissociated. The cells were maintained in tissue culture for up to 9 weeks in a synthetic serum-free media. XY99-5038 (100 ng/ml) or a vehicle was added to culture every 3-4 days, starting at the first week of culturing. The number of cells were counted and compared for each time point and treatment. Cell viability was also determined by MTT assay, whereas apoptotic cell death was evaluated by the TUNEL assay. XY99-5038 treatment significantly reduced cell loss, increased cell viability, and inhibited apoptosis in this long-term retinal neuronal culture. Our data also show that the protective effect of XY99-5038 is more potent than that of bFGF. Our data suggest that XY99-5038 could be beneficial to the prolongation of neuron survival.
3. Brain Res. 2004 May 1;1006(2):198-206.
Involvement of phosphatidylinositol 3-kinase and insulin-like growth factor-I in YXLST-mediated neuroprotection.
Yan X, Shen H, Zaharia M, Wang J, Wolf D, Li F, Lee GD, Cao W.
In the present study, we examine the neuroprotective role of the external Qi of YXLST in cultured retinal neurons. Primary retinal neuronal cultures were grown from retinas of 0-2-day-old Sprague-Dawley rats. Cultures were treated directly with external Qi of YXLST 30 min prior to H(2)O(2) exposure in most experiments. Cell viability was measured by 3,(4,5-dimethylthiazol-2-yl)2,5-diphenyl-tetrazolium bromide (MTT) assay. Apoptotic cell death was evaluated by the TdT-mediated digoxigenin-dUTP nick-end labeling TUNEL assay, and by DNA laddering analysis. Northern blot analysis was performed to examine the level of insulin-like growth factor-I (IGF-I) gene expression. Phosphatidylinositol 3-kinase (PI3K) assay was performed to study the PI3K activity. The results showed that treatment of external Qi of YXLST significantly attenuated neuronal death that was induced by 24-h exposure to hydrogen peroxide, and greatly inhibited hydrogen peroxide-induced apoptosis. External Qi of YXLST also upregulated IGF-I gene expression and increased PI3K activity. These observations indicate that external Qi-mediated IGF-I expression and PI3K signaling could be one of the mechanisms in neuroprotection by YXLST. |