【摘 要】
：
Purpose: The main purpose of this study was to investigate the active components of the Chinese medicine formula Shenqi San (SS) by HPLC-DAD-ESI-QTOF-MS,demonstrate the anticancer mechanism of SS on h
【机 构】
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Key Laboratory of Resources and Chemistry of Chinese Medicine, Hubei University of Chinese Medicine,
【出 处】
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德国(罗腾堡)第48届国际中医药大会(中国中医部分)
论文部分内容阅读
Purpose: The main purpose of this study was to investigate the active components of the Chinese medicine formula Shenqi San (SS) by HPLC-DAD-ESI-QTOF-MS,demonstrate the anticancer mechanism of SS on human lung adenocarcinoma A549 cells by evaluating the cell proliferation and apoptosis induction.Methods: The chloroform extraction of SS (CE-SS) was extracted from SS,while HPLC-DAD-ESI-QTOF-MS assay was performed to identified components of CE-SS.MTT assay was used to quantify the proliferation of A549 cells with the treatment of CE-SS.Apoptosis analysis was carried out by detecting phosphatidylserine (PS) externalization using the Annexin V-FITC Apoptosis Detection Kits and the stained cells were analyzed with a flow cytometer.DAPI staining assay was carried out to observe morphological characteristics of apoptotic ce11s.Western blot detected the expression of important signaling proteins involved apoptosis caspase-3,-8,-9,p53,Bax and Bcl-2.Results: Eight compounds were identified through HPLC-DAD-ESI-QTOF-MS analysis and 3-pyridine carboxylic acid,barbatin C,scutebarbatine F and barbatine D may be the main compounds responsible for the antitumor of CE-SS.The CE-SS suppress the proliferation of lung cancer A549 cells in a time and dose-dependent manner.By Annexin V-FITC/PI double staining,we can see that treatment with CE-SS induced apoptosis in A549 cells.After 24h exposure to CE-SS,the expression of protein cleaved-caspase-9,cleaved-caspase-8 and cleaved-caspase-3 were activated,the expression of protein p53 increased while the expression of Bax/Bcl-2 ratio also increased.Conclusion: This study identified the eight compounds of CE-SS,and demonstrated the anticancer effect on human lung adenocarcinoma A549 cells via induction of apoptosis.
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