Effects of catalpol on H<sub>2</sub>O<sub>2</sub>-induced osteoblast injury and its mechanism

DUAN Bo; CHEN Lichuan; MA Zhiyi; YU Zhao; LIU Jing; WANG Jinjun

doi:10.6039/j.issn.1001-0408.2024.10.12

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Effects of catalpol on H₂O₂-induced osteoblast injury and its mechanism

更新时间：2025-09-25

- Effects of catalpol on H₂O₂-induced osteoblast injury and its mechanism
- ZHONGGUO YAOFANG Vol. 35, Issue 10, Pages: 1220-1225(2024)
- 作者机构：
  
  武汉市中医医院风湿病科，武汉　430050
- 作者简介：
- 基金信息：
- DOI：10.6039/j.issn.1001-0408.2024.10.12
  CLC： R965
- Received：15 December 2023，
  
  Revised：2024-04-17，
  
  Accepted：18 April 2024，
  
  Published：30 May 2024
- 稿件说明：
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段波,陈丽川,马志毅,等.梓醇对H₂O₂诱导成骨细胞损伤的影响及机制[J].中国药房,2024,35(10):1220-1225.

DUAN Bo,CHEN Lichuan,MA Zhiyi,et al.Effects of catalpol on H₂O₂-induced osteoblast injury and its mechanism[J].ZHONGGUO YAOFANG,2024,35(10):1220-1225.
段波,陈丽川,马志毅,等.梓醇对H₂O₂诱导成骨细胞损伤的影响及机制[J].中国药房,2024,35(10):1220-1225. DOI： 10.6039/j.issn.1001-0408.2024.10.12.

DUAN Bo,CHEN Lichuan,MA Zhiyi,et al.Effects of catalpol on H₂O₂-induced osteoblast injury and its mechanism[J].ZHONGGUO YAOFANG,2024,35(10):1220-1225. DOI： 10.6039/j.issn.1001-0408.2024.10.12.

摘要

目的

探究梓醇对H

诱导成骨细胞损伤的影响及机制。

方法

将小鼠成骨细胞MC3T3-E1分为对照组、模型组、空载组（转染空载质粒）、梓醇组（100 μmol/L）、梓醇+叉头框蛋白O3（FoxO3）过表达组（100 μmol/L梓醇+转染FoxO3过表达质粒），经梓醇和转染处理后，除对照组细胞不作处理外，其余各组细胞以H

诱导建立成骨细胞氧化应激模型。检测各组细胞活力、凋亡率、碱性磷酸酶（ALP）活性、钙结节光密度（OD）值、活性氧（ROS）的平均荧光强度（MFI）、抗氧化酶[超氧化物歧化酶（SOD）、过氧化氢酶（CAT）

]

活性、炎症因子[白细胞介素6（IL-6）、IL-1β

]

水平、FoxO3/Wnt/

-连环蛋白（

-catenin）信号通路相关蛋白表达水平。

结果

与对照组比较，模型组细胞活力、ALP活性、钙结节OD值、抗氧化酶活性和Wnt、

-catenin蛋白表达水平均显著降低，凋亡率、ROS的MFI、炎症因子水平和FoxO3蛋白表达水平均显著升高（

＜0.05）；与模型组比较，空载组细胞上述指标均无明显变化（

＞0.05），梓醇组细胞上述指标均显著逆转（

＜0.05）；与梓醇组比较，梓醇+FoxO3过表达组细胞上述指标的逆转效果均被显著削弱（

＜0.05）。

结论

梓醇可通过下调FoxO3激活Wnt/

-catenin信号通路，抑制H

诱导的MC3T3-E1细胞氧化应激和炎症反应，提高细胞活力与成骨分化能力，抑制细胞凋亡。

Abstract

OBJECTIVE

To investigate the effects of catalpol on H

-induced osteoblast injury and its mechanism.

METHODS

The osteoblasts MC3T3-E1 were separated into control group， model group， empty group （transfected with empty plasmid）， catalpol group （100 μmol/L）， catalpol+forkhead box O3 （FoxO3） overexpression group （100 μmol/L catalpol+transfected with FoxO3 overexpression plasmid）. After catalpol treatment and transfection， except for control group， other groups were induced with H

to establish osteoblast oxidative stress model. The cell viability， apoptotic rate， alkaline phosphatase （ALP） activity， optical density （OD） value of calcium nodule， mean fluorescence intensity （MFI） of reactive oxygen species （ROS）， antioxidant enzyme activity [superoxide dismutase （SOD）， catalase （CAT）

]

， the levels of inflammatory factors [interleukin-6 （IL-6）， IL-1β

]

， and the expressions of FoxO3/Wnt/

-catenin signaling pathway-related proteins were detected in each group.

RESULTS

Compared with the control group， the cell viability， ALP activity， OD value of calcium nodule， activities of antioxidant enzyme， and the protein expressions of Wnt and

-catenin were decreased significantly in the model group， while apoptotic rate， MFI levels of ROS， inflammatory factor levels and the protein expression of FoxO3 were all increased significantly （

＜0.05）. Compared with the model group， above indicators of the empty group had no significant change （

＞0.05）， while those of catalpol group were reversed significantly （

＜0.05）. Compared with the catalpol group， the reversal effect of the changes in the above indicators was significantly weakened in the catalpo

l+FoxO3 overexpression group cells （

＜0.05）.

CONCLUSIONS

Catalpol can activate Wnt/

-catenin signaling pathway by down-regulating FoxO3， thereby inhibiting H

-induced MC3T3-E1 oxidative stress and inflammation reaction， enhancing cell viability and osteogenic differentiation activity， and alleviating apoptosis injury.

关键词

Keywords

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⁰

Effects of catalpol on H2O2-induced osteoblast injury and its mechanism

DOI：10.6039/j.issn.1001-0408.2024.10.12

摘要

Abstract

关键词

Keywords

references

Effects of catalpol on H₂O₂-induced osteoblast injury and its mechanism