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1.
Chinese Journal of Cancer Biotherapy ; (6): 988-992, 2019.
Article in Chinese | WPRIM | ID: wpr-793298

ABSTRACT

@# Objective: To investigate the effect of ginsenoside Rg3 combined with TRAIL on the apoptosis of lung cancer H358 cells and its possible mechanism. Methods: After the completion of cell culture, H538 cells were treated with TRAIL (0, 50, 100, 200 ng/ ml ) or Rg3 (0, 25, 50, 100 μmol/L) for 48 h, and the cells were grouped according to different treatments, namely control group, 50 μmol/LRg3 group, 100 ng/ml TRAILgroup and 50 μmol/LRg3+100 ng/ml TRAILgroup. The effects of Rg3 and/or TRAILon the proliferation of H358 cells were detected by MTT assay. The effects of Rg3 and/or TRAIL on the morphological changes of H358 cells were observed by DAPI staining. Theapoptosis of H358 cells in each group was detected by flow cytometry. The effects of Rg3 and/or TRAIL on the expressions of death receptor 5 (DR5) and caspase-8 in H358 cells were detected by WB. Results: Compared with the other groups, the proliferation of lung cancer H358 cells was significantly inhibited, while the apoptosis was significantly elevated in the 50 μmol/LRg3+100 ng/ml TRAILgroup (P<0.05).After color developing, cells in 50 μmol/LRg3+100 ng/ml TRAILgroup had nuclear shrinkage, chromatin condensation, increased fluorescence intensity, and late morphological changes such as saturation fragmentation. Compared with the other groups, the expression levels of DR5 and caspase-3 ,8 in the cells of 50 μmol/L Rg3+100 ng/ml TRAIL group were significantly increased (P<0.05). Conclusion: Ginsenoside Rg3 combined with TRAIL can synergistically inhibit the proliferation and induce apoptosis of lung cancer H358 cells. The mechanism may be related to the up-regulation of DR5 and caspase-8 by ginsenoside Rg3.

2.
Chinese Pharmaceutical Journal ; (24): 590-594, 2015.
Article in Chinese | WPRIM | ID: wpr-859400

ABSTRACT

OBJECTIVE: To investigate whether the ethanol extract of Oldenlandia diffusa (EEHD) have impact on the TGF-β1-induced epithelial mesenchymal transformation (EMT) of human lung adenocarcinoma cell H358 in vitro. METHODS: The cell model to study EMT of H358 cells was established with 5 ng·mL-1 TGF-β1 for 24 h. Then, after being mixed with low, medium and high concentration of EEHD respectively for 48 h, H358 cells were collected for detection of protein and mRNA expression of epithelial marker E-cadherin and mesenchymal cell marker vimentinby Western-Blot and quantitative PCR. RESULTS: The concentration of 5 ng·mL-1 TGF-β1 can successfully induce the transformation from epithelialphenotype to mesenchymal phenotype. The concentration of EEHD is positively correlated with increasing expression of E-cadherin, while negatively correlation with the decreasing expression of vimentin. CONCLUSION: The EEHD have partially reversal effect of epithelial mesenchymal transformation on lung adenocarcinoma cell induced by TGF-β1.

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