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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/28519


    標題: Baicalein, an active component of Scutellaria baicalensis Georgi, prevents lysophosphatidylcholine-induced cardiac injury by reducing reactive oxygen species production, calcium overload and apoptosis via MAPK pathways
    作者: Chen, Huai-Min
    Hsu, Jong-Hau
    Liou, Shu-Fen
    Chen, Tsan-Ju
    Chen, Li-Ying
    Chiu, Chaw-Chi
    Yeh, Jwu-Lai
    貢獻者: 藥學系
    關鍵字: Baicalein
    Lysophosphatidylcholine
    Apoptosis
    Reactive oxygen species
    Calcium
    日期: 2014-07
    上傳時間: 2015-05-06 21:19:12 (UTC+8)
    出版者: Biomed Central Ltd
    摘要: Background: Lysophosphatidylcholine (lysoPC), a metabolite from membrane phospholipids, accumulates in the ischemic myocardium and plays an important role in the development of myocardial dysfunction ventricular arrhythmia. In this study, we investigated if baicalein, a major component of Huang Qui, can protect against lysoPC-induced cytotoxicity in rat H9c2 embryonic cardiomyocytes. Methods: Cell viability was detected by the MTT assay; ROS levels were assessed using DCFH-DA; and intracellular free calcium concentrations were assayed by spectrofluorophotometer. Cell apoptosis and necrosis were evaluated by the flow cytometry assay and Hoechst staining. Mitogen-Activated Protein Kinases (MAPKs), which included the ERK, JNK, and p38, and the apoptotic mechanisms including Bcl-2/Bax, caspase-3, caspase-9 and cytochrome c pathways were examined by Western blot analysis. The activation of MAPKs was examined by enzyme-linked immunosorbent assay. Results: We found that lysoPC induced death and apoptosis of H9c2 cells in a dose-dependent manner. Baicalein could prevent lysoPC-induced cell death, production of reactive oxygen species (ROS), and increase of intracellular calcium concentration in H9c2 cardiomyoctes. In addition, baicalein also inhibited lysoPC-induced apoptosis, with associated decreased pro-apoptotic Bax protein, increased anti-apoptotic Bcl-2 protein, resulting in an increase in the Bcl-2/Bax ratio. Finally, baicalein attenuated lysoPC-induced the expression of cytochrome c, casapase-3, casapase 9, and the phosphorylations of ERK1/2, JNK, and p38. LysoPC induced ERK1/2, JNK, and p38 activations were inhibited by baicalein. Conclusions: Baicalein protects cardiomyocytes from lysoPC-induced apoptosis by reducing ROS production, inhibition of calcium overload, and deactivations of MAPK signaling pathways.
    Appears in Collections:[藥學系(所)] 期刊論文

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