Hou Y.,Lishui Country Peoples Hospital |
Hou Y.,Yangzhou University |
Yuan L.,Yangzhou University |
Yuan L.,97th Hospital of Peoples Liberation Army |
And 3 more authors.
Tumor | Year: 2011
Objective: To investigate the effect of Celastrus orbiculatus extracts (COE) on xenograft tumor growth of HepA1-6 hepatoma in mice, and to explore its possible mechanism. Methods: HepA1-6 hepatoma model was established in mice, and then these mice were randomly divided into blank control group, solvent control group (1% DMSO), negative control group (0.9% NaCl solution), positive control group (cisplatin), and low-, medium- and high-dose COE groups (10, 20 and 40 mg/kg, respectively). The body weight, tumor growth inhibitory rate, liver index, spleen index and thymus gland index were calculated, and the expression levels of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) as well as microvessel density (MVD) were detected by immunohistochemistry. The apoptosis rate was determined by TUNEL assay. Results: COE could significantly inhibit the tumor growth, increase the apoptosis rate, and down-regulate the expression levels of VEGF, bFGF and MVD of HepA1-6 hepatoma in the liver of mice, as compared with the negative control group (P < 0.05). There was no statistically significant differences in liver index, spleen index, thymus gland index and body weight between COE-treated groups and the negative control group (P > 0.05). Conclusion: COE can inhibit the xenograft tumor growth of HepA1-6 hepatoma in mice. This effect may be associated with the enhancement of apoptosis and the inhibition of angiogenesis in tumors. Copyright© 2011 by TUMOR.
Liu H.,97th Hospital of Peoples Liberation Army |
Yang Y.,97th Hospital of Peoples Liberation Army |
Cai X.,97th Hospital of Peoples Liberation Army |
Gao Y.,97th Hospital of Peoples Liberation Army |
And 2 more authors.
Pharmaceutical Biology | Year: 2015
Context: Rheumatoid arthritis fibroblast-like synoviocytes (RAFLSs) play an important role in the initiation and progression of RA, which are resistant to apoptosis and proliferate in an anchorage-independent manner. Objective: The effects of arctigenin on the proliferation and apoptosis of RAFLSs were explored. Materials and methods: Arctigenin (0-160 μM) was used to treat RAFLSs for 48 h. Cell viability and apoptosis were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide assay and annexin V/propidium iodide staining. Western blot analysis was performed to detect the changes in apoptosis-related genes. Results and discussion: Arctigenin decreased cell viability by 23, 30, and 38% at the dose of 10, 20, and 30 μM, respectively. The half maximal inhibitory concentration (IC50) of arctignein on RAFLSs was about 38 μM. Moreover, 9, 15, and 21% of RAFLSs are induced apoptosis by 10, 20, and 30 μM of arctigenin. The apoptotic response was due to the loss of mitochondrial membrane potential, coupled with the release of cytochrome C into cytoplasm, the up-regulation of pro-apoptotic protein, Bax, and down-regulation of antiapoptotic protein, B cell lymphoma 2 (Bcl-2). The activation of mitochondrial pathway in arctigenin-treated RAFLSs induced the cleavage of caspase-9, caspase-3, and poly (ADP-ribose) polymerase (PARP). Additionally, arctigenin inhibited the nuclear translocation of p65, decreased the degradation of inhibitor of kappa B alpha (IκBα), and attenuated the phosphorylation of Akt. Conclusion: Our results reveal that arctigenin inhibits cell proliferation and induces mitochondrial apoptosis of RAFLSs, which is associated with the modulation of NF-κB and Akt signaling pathways. © 2015 Informa Healthcare USA, Inc. All rights reserved.