目的 探讨微RNA（miR）-27a对人牙髓干细胞（hDPCs）低氧诱导因子1α（HIF-1α）及生物活性的影响，并基于PI3K/Akt信号通路探讨潜在的作用机制。方法 动物实验：30只SPF级雄性SD大鼠（6~9月龄，体重275~310 g ）随机分为正常组（Nor），牙髓炎组（Pul），空载组（NL），抑制剂组（Inh），抑制剂+740Y-P组（Inh+740Y-P），每组6只。Real time-PCR检测miR-27a表达水平，HE染色观察牙髓组织病理变化，ELISA检测相关炎症因子水平，免疫印迹法检测HIF-1α和PI3K/Akt信号通路相关蛋白表达水平。细胞实验：将hDPCs随机分为对照组（Ctrl），脂多糖组（LPS），阴性对照抑制剂组（NC inh），miR-27a抑制剂组（miR-27a inh），miR-27a抑制剂+740Y-P组（miR-27a inh+740Y-P）。CCK-8法和流式细胞术检测细胞增殖和凋亡率。结果 动物实验显示：与正常组相比，牙髓炎组和空载组大鼠牙髓组织中miR-27a、炎症因子白细胞介素（IL）-6、IL-1β、肿瘤坏死因子（TNF）-α、HIF-1α及PI3K/Akt信号通路相关蛋白水平均显著升高（P<0.05）。抑制剂组上述指标较牙髓炎组和空载组显著降低（P<0.05）。抑制剂+740Y-P组较抑制剂组，炎症因子、HIF-1α及PI3K/Akt信号通路相关蛋白水平显著升高（P<0.05）。细胞实验显示：随着LPS处理时间延长，hDPCs中miR-27a表达水平逐渐升高（P<0.05）。与Ctrl组相比，LPS组和NC inh组miR-27a、细胞凋亡率、炎症因子、HIF-1α蛋白及PI3K/Akt信号通路相关蛋白水平显著升高（P<0.05），细胞增殖率显著降低（P<0.05）。MiR-27a inh组较LPS组和NC inh组，上述指标显著降低（P<0.05），细胞增殖率显著升高（P<0.05）。MiR-27a inh+740Y-P组较miR-27a inh组，细胞凋亡率、炎症因子、HIF-1α蛋白及PI3K/Akt信号通路相关蛋白水平显著升高（P<0.05），细胞增殖率显著降低（P<0.05）。结论 MiR-27a可通过激活PI3K/Akt/HIF-1α信号通路，加剧炎症反应，影响牙髓干细胞的增殖、凋亡等生物活性，推动牙髓炎病情发展。

Objective To investigate the effects of microRNA(miR)-27a on hypoxia-inducible factor 1α (HIF-1α) and the biological activity of human dental pulp stem cells (hDPCs), and to preliminarily explore its potential mechanism based on the PI3K/Akt signaling pathway. Methods Animal experiments: Thirty SPF-grade male SD rats (6-9 months old, weighing 275-310 g) were randomly divided into five groups (n=6 per group): Normal group (Nor),pulpitis group (Pul), no-load group (NL), inhibitor group (Inh), Inh+740Y-P group. The expression level of miR-27a was detected by Real-time PCR. Pathological changes in pulp tissue were observed by HE staining. The levels of related inflammatory factors were detected by ELISA. The expression levels of HIF-1α and PI3K/Akt signaling pathway-related proteins were detected by Western blotting. Cell experiments: hDPCs were randomly divided into five groups, control group (Ctrl), lipopolysaccharidegroup (LPS), negative control inhibitor group（NC inh）, miR-27a inhibitor group (miR-27a inh), miR-27a inhibitor+740Y-P group (miR-27a inh+740Y-P). Cell proliferation and apoptosis rates were detected by CCK-8 assay and flow cytometry, respectively. Results Animal experiment: Compared with the Nor group, the levels of miR-27a, inflammatory cytokines interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α, HIF-1α, and proteins related to the PI3K/Akt signaling pathway in the Pul and NL groups increased significantly (P<0.05). The above-mentioned indicators in the Inh group were significantly lower than those in the Pul and NL groups (P< 0.05). Compared with the Inh group, the levels of inflammatory cytokines, HIF-1α, and proteins related to the PI3K/Akt signaling pathway in the Inh+740Y-P group increased significantly (P<0.05). Cell experiments: With the prolongation of LPS treatment time, the expression level of miR-27a in hDPCs gradually increased (P<0.05). Compared with the Ctrl group, the levels of miR-27a, cell apoptosis rate, inflammatory cytokines, HIF-1α protein, and proteins related to the PI3K/Akt signaling pathway in the LPS group and NC inh group increased significantly (P<0.05), while the cell proliferation rate decreased significantly (P<0.05). Compared with the LPS group and NC inh group, the above-mentioned indicators in the miR-27a inh group decreased significantly (P<0.05), and the cell proliferation rate increased significantly (P<0.05). Compared with the miR-27a inh group, the cell apoptosis rate, inflammatory cytokines, HIF-1α protein, and proteins related to the PI3K/Akt signaling pathway in the miR-27a inh + 740Y-P group increased significantly (P<0.05), while the cell proliferation rate decreased significantly (P<0.05). Conclusion MiR-27a can exacerbate the inflammatory response by activating the PI3K/Akt/HIF-1α signaling pathway, thereby affecting the biological activities such as proliferation and apoptosis of dental pulp stem cells and promoting the progression of pulpitis in rats.