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Rosiglitazone enhanced growth inhibition of cisplatin in hunman lung adenocarcinoma cell

Ting Fang, Zhuang Ying-zhi, Jianguo Cao

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Abstract

Aim To investigate the synergistic effect of the ligand o f Peroxisome Proliferator-activated Receptor gamma Rosiglitazone with Cisplatin in vitro on human lung adenocarcinoma cell proliferation inhibition and its possible mechanism. Methods Human lung adenocarcinoma A549 cell line was cultured in vitro, cytotoxicity assay was tested by MTT assay. The influ ence of Rosiglitazone with Cisplatin on human lung carcinoma cell apoptosis was detected by PI staning flow cytometry and AO/EB double fluorescence stain. The c hanges of expression of PPARγ and Bcl-2 protein in lung carcinoma cells betwee n untreated and treated with Rosiglitazone were observed by immunohistochemistry . Results Rosiglitazone at various concentrations (1.25, 2.5 μmo l·L -1)enhanced the growth inhibitory effect of Cisplatin to A549 cells( P1.15). Rosiglitazone at the concentration of 1.25 μmol·L -1 augme nted the induction apoptosis of A549 cells by treatment with Cisplatin at variou s concentrations of 1.98 mg·L -1, 2.8 mg·L -1 and 4.0 mg·L -1 . A549 cells treated with Rosiglitazone at concentration of 1.25 μmol·L -1 domostrated nuclear traslocations of PPARγ protein and down-regulation of Bcl-2 protein. Conclusion The ligand of PPARγ Rosiglitazone enhanc ed the inhibition of proliferation and induction of apoptosis by treatment with Cisplatin in A549 cells cultured in vitro. Activation of PPARγ protein and the down-regulation of Bcl-2 possiblely play an improtant role in chemosenstiz eic mechanism of Rosiglitazone in vitro.

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Aim To investigate the synergistic effect of the ligand o f Peroxisome Proliferator-activated Receptor gamma Rosiglitazone with Cisplatin in vitro on human lung adenocarcinoma cell proliferation inhibition and its possible mechanism. Methods Human lung adenocarcinoma A549 cell line was cultured in vitro, cytotoxicity assay was tested by MTT assay. The influ ence of Rosiglitazone with Cisplatin on human lung carcinoma cell apoptosis was detected by PI staning flow cytometry and AO/EB double fluorescence stain. The c hanges of expression of PPARγ and Bcl-2 protein in lung carcinoma cells betwee n untreated and treated with Rosiglitazone were observed by immunohistochemistry . Results Rosiglitazone at various concentrations (1.25, 2.5 μmo l·L -1)enhanced the growth inhibitory effect of Cisplatin to A549 cells( P1.15). Rosiglitazone at the concentration of 1.25 μmol·L -1 augme nted the induction apoptosis of A549 cells by treatment with Cisplatin at variou s concentrations of 1.98 mg·L -1, 2.8 mg·L -1 and 4.0 mg·L -1 . A549 cells treated with Rosiglitazone at concentration of 1.25 μmol·L -1 domostrated nuclear traslocations of PPARγ protein and down-regulation of Bcl-2 protein. Conclusion The ligand of PPARγ Rosiglitazone enhanc ed the inhibition of proliferation and induction of apoptosis by treatment with Cisplatin in A549 cells cultured in vitro. Activation of PPARγ protein and the down-regulation of Bcl-2 possiblely play an improtant role in chemosenstiz eic mechanism of Rosiglitazone in vitro.

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Available abstract

Aim To investigate the synergistic effect of the ligand o f Peroxisome Proliferator-activated Receptor gamma Rosiglitazone with Cisplatin in vitro on human lung adenocarcinoma cell proliferation inhibition and its possible mechanism. Methods Human lung adenocarcinoma A549 cell line was cultured in vitro, cytotoxicity assay was tested by MTT assay. The influ ence of Rosiglitazone with Cisplatin on human lung carcinoma cell apoptosis was detected by PI staning flow cytometry and AO/EB double fluorescence stain. The c hanges of expression of PPARγ and Bcl-2 protein in lung carcinoma cells betwee n untreated and treated with Rosiglitazone were observed by immunohistochemistry . Results Rosiglitazone at various concentrations (1.25, 2.5 μmo l·L -1)enhanced the growth inhibitory effect of Cisplatin to A549 cells( P1.15). Rosiglitazone at the concentration of 1.25 μmol·L -1 augme nted the induction apoptosis of A549 cells by treatment with Cisplatin at variou s concentrations of 1.98 mg·L -1, 2.8 mg·L -1 and 4.0 mg·L -1 . A549 cells treated with Rosiglitazone at concentration of 1.25 μmol·L -1 domostrated nuclear traslocations of PPARγ protein and down-regulation of Bcl-2 protein. Conclusion The ligand of PPARγ Rosiglitazone enhanc ed the inhibition of proliferation and induction of apoptosis by treatment with Cisplatin in A549 cells cultured in vitro. Activation of PPARγ protein and the down-regulation of Bcl-2 possiblely play an improtant role in chemosenstiz eic mechanism of Rosiglitazone in vitro.

Key concepts: Rosiglitazone, Cisplatin, Apoptosis, A549 cell, Cell growth, MTT assay, Chemistry, Flow cytometry

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