文章摘要
黄芩苷通过PI3K/AKT/mTOR信号通路促进胶质瘤细胞U251凋亡与自噬作用及机制研究
Baicalin promotes apoptosis and autophagy of GLIoma U251 cells through PI3K/AKT/mTOR signaling pathway and its mechanismFAN Qiong1, LIU Hua1, XU Dongmei1, ZHONG Bo2 (1.Xinyu People"s Hospital of Jiangxi Department of Rehabilitation Medicine, 2. Xinyu People"s Hospital of Jiangxi Department of Neurosurgery, Xinyu 338000, Jiangxi, China)
DOI:
中文关键词: 黄芩苷  神经胶质瘤  PI3K/AKT/mTOR  凋亡  自噬
英文关键词: baicalin  Glioma  PI3K/AKT/mTOR  Apoptosis  Autophagy
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作者单位邮编
樊琼 江西省新余市人民医院康复医学科 338000
刘华 江西省新余市人民医院康复医学科 
徐冬梅 江西省新余市人民医院康复医学科 
钟波 江西省新余市人民医院神经外科 
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中文摘要:
      目的:探讨黄芩苷对神经胶质瘤细胞U251凋亡与自噬的作用及机制。方法:以不同浓度的黄芩苷( 0、50、75、100μg /mL) 处理胶质瘤细胞U251;采用CCK-8法检测黄芩苷对神经胶质瘤细胞U251活性的影响;流式细胞术检测药物对U251细胞凋亡; Western blot 检测神经胶质瘤细胞U251蛋白的表达;RT-PCR检测神经胶质瘤细胞U251 RNA的表达。结果:黄芩苷以剂量和时间依赖性方式抑制神经胶质瘤细胞 U251的增殖,随着黄芩苷药物浓度的增加,p-PI3K、p-AKT和p-mTOR 的表达降低,凋亡相关蛋白cleaved-caspase-3 和 Bax 的表达增加,而 Bcl-2 的表达降低。自噬相关蛋白 LC3II、beclin1增加,而p62显著减少。结论:黄芩苷通过通过PI3K/AKT/mTOR信号通路促进胶质瘤细胞U251凋亡与自噬,其具有抑制胶质瘤的作用,临床上值得推广。
英文摘要:
      Objective: To investigate the effect and mechanism of baicalin on apoptosis and autophagy of U251 glioma cells. Methods: Glioma cells U251 were treated with different concentrations of baicalin (0, 50, 75, 100μg /mL). The effect of baicalin on U251 activity of glioma cells was detected by CCK-8 assay. Apoptosis of U251 cells was detected by flow cytometry. The expression of U251 protein in glioma cells was detected by Western blot. Expression of U251RNA in glioma cells was detected by RT-PCR. Results: Baicalin inhibits the proliferation of glioma cells U251 in a dose-dependent and time-dependent manner. With the increase of baicalin concentration, the expression of p-PI3K, p-Akt, and p-mTOR decreased, and the expression of apoptosis-related proteins Cleaved-caspase-3 and Bax increased. Bcl-2 expression was decreased. Autophagy related proteins LC3II and Beclin1 increased, while P62 decreased significantly. Conclusion: Baicalin can promote apoptosis and autophagy of U251 glioma cells through PI3K/AKT/mTOR signaling pathway, which has the effect of inhibiting glioma and is worthy of clinical promotion.
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