黄芩苷通过PI3K/AKT信号轴调控牙髓干细胞增殖及血管生成的机制研究

doi:10.13701/j.cnki.kqyxyj.2026.02.008

摘要/Abstract

摘要： 目的: 牙髓干细胞(dental pulp stem cells,DPSC)在牙髓修复和再生方面的潜在应用受到了越来越多的关注,同时,在多种疾病模型中,黄芩苷展现出抗炎、抗肿瘤、保护组织损伤等多重生物学效应。然而,黄芩苷在DPSC中的影响作用仍不明确。因此,本研究旨在探索黄芩苷对DPSC增殖和血管生成的作用机制,并探讨磷脂酰肌醇3-激酶(phosphatidylinositol 3-kinase,PI3K)/蛋白激酶B(protein kinase B,AKT)信号轴在此过程中的调控机制。方法: 培养人DPSC,根据黄芩苷浓度其分为对照组(完全培养基)、10 μmol/L组、20 μmol/L组、50 μmol/L组和100 μmol/L组(完全培养基+不同浓度黄芩苷),观察不同浓度黄芩苷对DPSC细胞活性的影响,并进一步探讨PI3K/AKT信号轴的变化,同时在50 μmol/L组中添加LY294002(PI3K/AKT抑制剂)干预,观察其对DPSC细胞增殖和血管生成的调控作用。结果: (1)黄芩苷能提高DPSC的活性,抑制其凋亡,并且在50 μmol/L组中更为明显(P<0.05);(2)与其他各组相比,50 μmol/L组细胞中的PI3K、AKT mRNA以及p-PI3K/PI3K、p-AKT/AKT表达明显升高(P<0.05);(3)与50 μmol/L组相比,50 μmol/L+LY294002组DPSC细胞的增殖能力明显减弱、迁移个数明显减少(P<0.05),血管内皮生长因子(vascular endothelial growth factor,VEGF)、血管生成素-2(angiopoietin-2,Ang-2)表达明显降低。结论: 黄芩苷能够促进DPSC增殖和血管生成,这一过程与激活PI3K/AKT信号通路并提高VEGF、Ang-2的表达水平有关,为黄芩苷在DPSC中的应用提供了理论支持。

关键词: 黄芩苷, 牙髓干细胞, 细胞增殖, 血管生成, 调控机制

Abstract: Objective: To explore the effect of baicalin on the proliferation and angiogenesis of dental pulp stem cells (DPSC), and to investigate the regulatory mechanism of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signal axis in this process. Methods: Human DPSC were cultured and divided into the control group (complete medium), the 10 μmol/L group, the 20 μmol/L group, the 50 μmol/L group, and the 100 μmol/L group (complete medium + different concentrations of baicalin) according to the concentration of baicalin. The effect of different concentrations of baicalin on the viability of DPSC was observed. The changes of the PI3K/AKT signaling axis were further explored. Meanwhile, LY294002 (a PI3K/AKT inhibitor) was added to the 50 μmol/L group to observe its regulatory effect on the proliferation and angiogenesis of DPSC. Results: Baicalin could enhance the activity of DPSC, inhibit their apoptosis, and the effect was more obvious in the 50 μmol/L group (P<0.05). Compared with other groups, the expressions of PI3K, AKT mRNA, p-PI3K/PI3K, and p-AKT/AKT in the 50 μmol/L group were significantly increased (P<0.05). Compared with the 50 μmol/L group, the proliferation ability of DPSC in the 50 μmol/L+LY294002 group was significantly weakened and the number of migrations was significantly reduced. The expressions of vascular endothelial growth factor (VEGF) and angiopoietin-2 (Ang-2) were significantly decreased. Conclusion: Baicalein can promote the proliferation and angiogenesis of DPSC. This process is related to the activation of the PI3K/AKT signaling pathway and the increased expression levels of VEGF and Ang-2, providing theoretical support for the application of baicalein in DPSC.

Key words: baicalin, dental pulp stem cells, cell proliferation, angiogenesis, regulatory mechanism

程刚, 吴修胤, 李月秀, 米静, 武岐山. 黄芩苷通过PI3K/AKT信号轴调控牙髓干细胞增殖及血管生成的机制研究[J]. 口腔医学研究, 2026, 42(2): 126-133.

CHENG Gang, WU Xiuyin, LI Yuexiu, MI Jing, WU Qishan. Study on Mechanism of Baicalin Regulating Proliferation and Angiogenesis of Dental Pulp Stem Cells through PI3K/AKT Signaling Axis[J]. Journal of Oral Science Research, 2026, 42(2): 126-133.

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