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| 补骨脂酚抗氧化应激保护细胞成骨分化机制研究 |
| Study on the mechanism of bakuchiol protecting osteogenic differentiation of cells via anti-oxidative stress |
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| DOI：10.3969/j.issn.1006-7108.2026.08.001 |
| 中文关键词: 补骨脂酚 抗氧化应激 成骨分化 |
| 英文关键词:bakuchiol oxidative stress osteogenic differentiation |
| 基金项目:国家自然科学基金（82274551）；广东省基础与应用基础研究基金（2023B1515230001） |
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| 中文摘要: |
| 目的 探讨补骨脂酚减轻MC3T3-E1细胞氧化应激损伤的机制，以及对氧化损伤的MC3T3-E1细胞的增殖、分化的影响。方法 将采购的MC3T3-E1细胞分为4组：对照组（普通生长培养基）、模型组（普通生长培养基 + 氧化损伤）、补骨脂酚组（含补骨脂酚的培养基 + 氧化损伤）、抑制剂组（含补骨脂酚的培养基 + ML385 + 氧化损伤）。模型组、补骨脂酚组和抑制剂组MC3T3-E1细胞经含200 μmol/L H2O2的生长培养基诱导氧化损伤模型。干预1、3、7 d 后通过CCK-8法检测补骨脂酚对氧化损伤的MC3T3-E1细胞活性的影响；在造模后干预第4天进行ROS检测；在诱导后第7天采用碱性磷酸酶染色检测成骨细胞碱性磷酸酶的活性；Western blot检测Nrf2、HO-1、SOD1、GPX1、CAT抗氧化应激相关蛋白与RUNX2、ALP、OPN等成骨相关蛋白的表达情况。结果 ①1 μmol/L补骨脂酚可促进氧化损伤的MC3T3-E1细胞增殖；②ROS荧光结果表明补骨脂酚可降低氧化应激损伤细胞中的活性氧水平；碱性磷酸酶染色结果表明补骨脂酚对受氧化应激损伤细胞的分化具有促进作用；③与模型组相比，补骨脂酚组 Nrf2、HO-1、SOD1、GPX1、CAT、RUNX2、ALP、OPN 蛋白表达显著上调（P<0.01）；与补骨脂酚组相比，抑制剂组上述蛋白表达显著下调（P<0.01）。结论 补骨脂酚对 H2O2 诱导的 MC3T3-E1 细胞氧化应激损伤具有保护作用，且能够促进损伤的 MC3T3-E1 细胞增殖与分化，其机制可能与促进Nrf2、HO-1、SOD1、GPX1、CAT抗氧化应激蛋白表达并激活RUNX2/ALP/OPN成骨相关通路有关。 |
| 英文摘要: |
| Objective To investigate the mechanism by which bakuchiol alleviates oxidative stress-induced injury in MC3T3-E1 cells and its effects on the proliferation and differentiation of oxidatively damaged MC3T3-E1 cells. Methods MC3T3-E1 cells were divided into four groups: a control group (cultured in standard growth medium), a model group (oxidative injury induced by H?O?), a bakuchiol group (H?O?-induced injury with bakuchiol treatment), and an inhibitor group (H?O? + bakuchiol + ML385). Oxidative stress was induced in the model, bakuchiol, and inhibitor groups by culturing the cells in growth medium containing 200 μmol/L H?O?. After 1, 3, and 7 days of treatment, cell viability was assessed using the CCK-8 assay. Intracellular reactive oxygen species (ROS) levels were measured on day 4 post-induction. Alkaline phosphatase (ALP) staining was performed on day 7 to evaluate osteoblast differentiation. Western blot analysis was used to detect the expression of antioxidant-related proteins (Nrf2、HO-1、SOD1, GPX1, CAT) and osteogenesis-related proteins (RUNX2, ALP, OPN). Results ① Bakuchiol at 1 μmol/L significantly promoted the proliferation of MC3T3-E1 cells under oxidative stress. ②ROS fluorescence analysis showed that bakuchiol reduced intracellular ROS levels. ALP staining indicated that bakuchiol enhanced osteogenic differentiation in oxidatively damaged cells. ③Compared with the model group, the bakuchiol group showed significantly increased expression of Nrf2、HO-1、SOD1, GPX1, CAT, RUNX2, ALP, and OPN proteins (P<0.01). Compared with the bakuchiol group, the inhibitor group showed a significant decrease in these protein levels (P<0.01). Conclusion Bakuchiol exerts a protective effect against H?O?-induced oxidative stress in MC3T3-E1 cells and promotes the proliferation and osteogenic differentiation of damaged cells. The underlying mechanism may involve the upregulation of antioxidant proteins (NRF2, HO-1, SOD1, GPX1, CAT) and activation of the RUNX2/ALP/OPN osteogenic signaling pathway. |
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