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- W2402214262 abstract "To explore the mechanism of ginsenoside Rh2 in reversing the resistance of lung adenocarcinoma cells to cisplatin.In the Rh2, DDP and DDP + Rh2 group A549DDP cells were treated with Rh2, cisplatin, cisplatin + Rh2 respectively for 48 hours. In the control group the A549DDP cells were not treated with any kind of drugs. The state of mitochondrial permeability transition pore (PTP) was evaluated by ultra violate spectrofluorometer. Concentration of calcium in cells, membrane potential of mitochondrion and apoptosis cells were determined by flow cytometry. The expression of cyt-c and Caspase-3 was estimated by Western blots. Cellular shapes were observed by fluorescent microscopy.The concentrations of calcium were similar among the former three groups, but was obviously increased in the Rh2 + DDP group (t = 22.47, P < 0.01). A(540) of mitochondrion among the former three groups were not different, but decreased significantly in the Rh2 + DDP group (t = 8.21, P < 0.01). The membrane potentials of mitochondrion showed no difference in the former groups, that was remarkably lower in the Rh2 + DDP group than in the control group (chi(2) = 46.01, P < 0.01). There was little expression of cty-c and Caspase-3 in the former groups, but high expression of those in the Rh2 + DDP group. Fluorescence was distributed equally on the cells nucleus in the former groups. In the Rh2 + DDP group many cell nucleus shrank or were distorted. The apoptosis rate of the cells was 6.32%, 7.24%, 7.41% and 21.96% in the four groups respectively. Which in Rh2 + DDP group was higher than that in the control group (t = 10.92, P < 0.05).The effect of ginsenoside Rh2 reversing resistance of lung adenocarcinoma A549DDP cells to cisplatin can be performed by apoptotic mitochondria pathway." @default.
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- W2402214262 date "2010-01-26" @default.
- W2402214262 modified "2023-09-23" @default.
- W2402214262 title "[Research on the mechanism of ginsenoside Rh2 reversing the resistance of lung adenocarcinoma cells to cisplatin]." @default.
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