梓醇对H2O2诱导成骨细胞损伤的影响及机制
R965; 目的 探究梓醇对H2O2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H2O2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...
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| Published in | 中国药房 Vol. 35; no. 10; pp. 1220 - 1225 |
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| Main Authors | , , , , , |
| Format | Journal Article |
| Language | Chinese |
| Published |
武汉市中医医院风湿病科,武汉 430050
01.05.2024
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1001-0408 |
| DOI | 10.6039/j.issn.1001-0408.2024.10.12 |
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| Abstract | R965; 目的 探究梓醇对H2O2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H2O2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/β-连环蛋白(β-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、β-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(P＜0.05);与模型组比较,空载组细胞上述指标均无明显变化(P＞0.05),梓醇组细胞上述指标均显著逆转(P＜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(P＜0.05).结论 梓醇可通过下调FoxO3激活Wnt/β-catenin信号通路,抑制H2O2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. |
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| AbstractList | R965; 目的 探究梓醇对H2O2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H2O2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/β-连环蛋白(β-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、β-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(P＜0.05);与模型组比较,空载组细胞上述指标均无明显变化(P＞0.05),梓醇组细胞上述指标均显著逆转(P＜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(P＜0.05).结论 梓醇可通过下调FoxO3激活Wnt/β-catenin信号通路,抑制H2O2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_FL | OBJECTIVE To investigate the effects of catalpol on H2O2-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 H2O2 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/β-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 β-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(P<0.05).Compared with the model group,above indicators of the empty group had no significant change(P>0.05),while those of catalpol group were reversed significantly(P<0.05).Compared with the catalpol group,the reversal effect of the changes in the above indicators was significantly weakened in the catalpol+FoxO3 overexpression group cells(P<0.05).CONCLUSIONS Catalpol can activate Wnt/β-catenin signaling pathway by down-regulating FoxO3,thereby inhibiting H2O2-induced MC3T3-E1 oxidative stress and inflammation reaction,enhancing cell viability and osteogenic differentiation activity,and alleviating apoptosis injury. |
| Author | 段波 喻昭 王进军 刘静 陈丽川 马志毅 |
| AuthorAffiliation | 武汉市中医医院风湿病科,武汉 430050 |
| AuthorAffiliation_xml | – name: 武汉市中医医院风湿病科,武汉 430050 |
| Author_FL | MA Zhiyi CHEN Lichuan LIU Jing YU Zhao DUAN Bo WANG Jinjun |
| Author_FL_xml | – sequence: 1 fullname: DUAN Bo – sequence: 2 fullname: CHEN Lichuan – sequence: 3 fullname: MA Zhiyi – sequence: 4 fullname: YU Zhao – sequence: 5 fullname: LIU Jing – sequence: 6 fullname: WANG Jinjun |
| Author_xml | – sequence: 1 fullname: 段波 – sequence: 2 fullname: 陈丽川 – sequence: 3 fullname: 马志毅 – sequence: 4 fullname: 喻昭 – sequence: 5 fullname: 刘静 – sequence: 6 fullname: 王进军 |
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| DocumentTitle_FL | Effects of catalpol on H2O2-induced osteoblast injury and its mechanism |
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| Keywords | catalpol inflammatory factor FoxO3/Wnt/β-catenin signaling pathway 氧化应激 炎症因子 osteogenic differentiation FoxO3/Wnt/β-catenin信号通路 梓醇 成骨分化 oxidative stress |
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| Snippet | R965; 目的 探究梓醇对H2O2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... |
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| Title | 梓醇对H2O2诱导成骨细胞损伤的影响及机制 |
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