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作 者:刘惠莉 LIU Huili(450007, Department of Stomatology, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Chin)
机构地区:[1]郑州大学附属郑州中心医院口腔科,450007
出 处:《实用口腔医学杂志》2018年第2期164-167,共4页Journal of Practical Stomatology
摘 要:目的:研究Akt/PKB信号通路对缺氧诱导的人牙周膜成纤维细胞(h PDLFs)凋亡的影响。方法:用MTT法、流式细胞术、q RT-PCR、Western blot、Lipofectamin 2000转染技术等测定hPDLFs在常氧和缺氧条件下的细胞增殖率、凋亡率、Akt/PKB信号通路和HIF-1α的表达。结果:与常氧条件相比,缺氧显著提高HIF-1α的表达,抑制细胞增殖并促进其凋亡,同时抑制Akt/PKB信号通路。在缺氧的条件下,抑制Akt/PKB信号通路的表达能够且显著抑制hPDLFs的增殖并促进其凋亡。结论:抑制Akt/PKB信号通路能促进缺氧诱导的hPDLFs凋亡。Objective: To investigate the effects of the Akt/PKB signaling pathway on hypoxia-induced apoptosis. Methods: The cell proliferation, apoptosis, Akt/PKB signaling pathway and HIF-1 a expression in periodontal ligament fibroblasts (hPDLFs) under normoxic and hypoxic conditions were evaluated by MTT assay, flowoytometry, qRT-PCR, Western blot and Lipofectamin 2000 transfection respectively. Results: The cell proliferation and the Akt/PKB pathway in hPDLFs were inhibited by hypoxia. Hypoxia promoted apoptosis and increased the levels of HIF- 1 a of hPDLFs. Akt/PKB signaling pathway inhibition inhibited cell proliferation and promoted hypoxia-induced apoptosis of hPDLFs. Conclusion: The inhibition of Akt/PKB signaling pathway may promote hypox- ia-induced apoptosis of hPDLFs under hyoxia condtition.
关 键 词:Akt/PKB信号通路 缺氧 人牙周膜成纤维细胞(hPDLFs) 细胞凋亡
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