目的 探讨黄芩素调节核因子κB抑制蛋白激酶（IKK）/核转录因子-κB（NF-κB）通路对脂多糖诱导的人牙髓干细胞细胞增殖和凋亡的影响。方法 将人牙髓干细胞分为对照组、模型组、黄芩素（2.5、5.0、10.0 μg/mL）组、黄芩素＋pCMV-NC组、黄芩素＋pCMV-IKK2EE组。检测人牙髓干细胞450 nm波长处的吸光度（A₄₅₀）值、EdU阳性率、凋亡率；ELISA检测人牙髓干细胞上清液白细胞介素（IL）-6、IL-8、肿瘤坏死因子-α（TNF-α）、IL-1β含量；qRT-PCR检测人牙髓干细胞中增殖细胞核抗原（PCNA）、细胞周期蛋白D1（CyclinD1）、Bcl-2相关X蛋白（Bax）、半胱天冬酶-3（Caspase-3）、B细胞淋巴瘤-2蛋白（Bcl-2）mRNA表达；Western blotting检测人牙髓干细胞中IKK/NF-κB通路蛋白表达；免疫荧光染色检测人牙髓干细胞中NF-κB p65核转移。结果 与模型组比较，黄芩素（2.5、5.0、10.0 μg/mL）组人牙髓干细胞A₄₅₀值、EdU阳性率、PCNA、CyclinD1、Bcl-2 mRNA表达显著升高，凋亡率、上清液IL-6、IL-8、TNF-α、IL-1β含量、Bax、Caspase-3 mRNA表达、p-IKK2/IKK2、p-IκBα/核因子κB抑制蛋白α（IκBα）、p-NF-κB p65/NF-κB p65蛋白表达、NF-κB p65核转移阳性率显著降低（P＜0.05）；pCMV-IKK2EE逆转了黄芩素10.0 μg/mL组对脂多糖诱导的人牙髓干细胞增殖抑制、凋亡促进及炎症反应的改善作用。结论 黄芩素能够通过抑制IKK/NF-κB信号通路，减轻脂多糖诱导的人牙髓干细胞炎症反应，恢复细胞增殖活力并抑制细胞凋亡。

Objective To investigate the effects of baicalein on lipopolysaccharide induced proliferation and apoptosis of hDPSCs by regulating IKK/NF-κB pathway. Methods Human dental pulp stem cells (hDPSCs) were divided into control group, model group, baicalein (2.5, 5.0, 10.0 μg/mL) group, baicalein + pCMV-NC group, and baicalein + pCMV-IKK2EE group. The A₄₅₀ value, EdU positive rate, and apoptosis rate of hDPSCs were measured. Content of IL-6, IL-8, TNF-α, and IL-1β in the supernatant of hDPSCs cells were detected by ELISA. The mRNA expressions of PCNA, CyclinD1, Bax, Caspase 3, and Bcl-2 in hDPSCs were detected by qRT-PCR. The protein expression of the IKK/NF-κB pathway in hDPSCs cells was detected by Western blotting. The nuclear translocation of NF-κB p65 in hDPSCs cells was detected by immunofluorescence staining. Results Compared with the model group, baicalein (2.5, 5.0, 10.0 μg/mL) group group were increased A₄₅₀ value, EdU positive rate, and mRNA expressions of PCNA, CyclinD1, and Bcl-2, while the apoptosis rate, supernatant levels of IL-6, IL-8, TNF-α, and IL-1β, mRNA expressions of Bax and Caspase 3, protein expressions of p-IKK2/IKK2, p-IκBα/IκBα, p-NF-κB p65/NF-κB p65, and the positive rate of NF-κB p65 nuclear translocation were decreased (P < 0.05). pCMV-IKK2EE reversed the ameliorative effects of baicalein 10.0 μg/mL group on lipopolysaccharide-induced proliferation inhibition, apoptosis promotion, and inflammatory response in hDPSCs cells. Conclusion Baicalein alleviates lipopolysaccharide-induced inflammatory response, restores cell proliferation activity, and inhibits cell apoptosis in hDPSCs cells by suppressing the IKK/NF-κB signaling pathway.

R287.7

山西省回国留学人员科研资助项目（2022-999）