胡黄连苷Ⅱ调节RIP1/RIP3/MLKL信号对地塞米松诱导成骨细胞凋亡的影响
The effect of picroside Ⅱ on dexamethasone-induced apoptosis of osteoblasts by regulating RIP1/RIP3/MLKL signal
  
DOI:10.3969/j.issn.1006-7108.2024.05.007
中文关键词:  胡黄连苷Ⅱ  RIP1/RIP3/MLKL  DEX  成骨细胞  凋亡
英文关键词:picroside II  RIP1/RIP3/MLKL  DEX  osteoblast  apoptosis
基金项目:郴财教指[(2020)35号,ZDYF2020177]
作者单位
陈鹏 李杨* 欧阳鹏辉 湖南省郴州市湘南学院附属医院(临床学院)骨二科湖南 郴州 423000 
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中文摘要:
      目的 探讨胡黄连苷Ⅱ调节受体相互作用蛋白激酶(RIP)1/RIP3/混合系列蛋白激酶样结构域(MLKL)信号对地塞米松(DEX)诱导成骨细胞凋亡的影响。方法 体外培养hFOB 1.19细胞,随机分为对照组、DEX组、DEX+胡黄连苷Ⅱ组、DEX+RIP1过表达组、DEX+空载质粒组、DEX+胡黄连苷Ⅱ+RIP1过表达组,分组处理后检测各组细胞活力、凋亡率、活性氧(ROS)相对水平、乳酸脱氢酶(LDH)、白细胞介素(IL)-1β、肿瘤坏死因子-α(TNF-α)及IL-6释放量、BCL-2及BAX相对表达、RIP1/RIP3/MLKL信号蛋白表达。结果 与对照组相比,DEX组细胞活力、BCL-2相对表达降低(P<0.05),凋亡率、ROS相对水平、LDH及IL-1β、TNF-α、IL-6释放量、细胞BAX及RIP1、RIP3、MLKL蛋白相对表达升高(P<0.05)。与DEX组相比,DEX+胡黄连苷Ⅱ组细胞活力、BCL-2相对表达升高(P<0.05),凋亡率、ROS相对水平、LDH及IL-1β、TNF-α、IL-6释放量、细胞BAX及RIP1、RIP3、MLKL蛋白相对表达降低(P<0.05);DEX+RIP1过表达组细胞活力、BCL-2相对表达降低(P<0.05),凋亡率、ROS相对水平、LDH及IL-1β、TNF-α、IL-6释放量、细胞BAX及RIP1、RIP3、MLKL蛋白相对表达升高(P<0.05);DEX+空载质粒组细胞各指标差异无统计学意义(P>0.05);过表达RIP1可减弱胡黄连苷Ⅱ对DEX诱导的hFOB 1.19细胞的作用。结论 胡黄连苷Ⅱ可通过下调RIP1/RIP3/MLKL通路而减轻炎症,从而抑制DEX诱导的成骨细胞凋亡。
英文摘要:
      Objective To investigate the effect of picroside II on dexamethasone (DEX)-induced osteoblast apoptosis by regulating the receptor-interacting protein (RIP) 1/RIP3/mixed lineage kinase domain-like (MLKL) signal. Methods HFOB 1.19 cells were cultured in vitro and randomly grouped into control group, DEX group, DEX+picroside II group, DEX+RIP1 overexpression group, DEX+empty plasmid group, and DEX+picroside II+RIP1 overexpression group. After grouping treatment, cell viability rate, apoptosis rate, the relative level of reactive oxygen species (ROS), the releases of lactate dehydrogenase (LDH), interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), IL-6, the relative expressions of BCL-2 and BAX, the expressions of RIP1/RIP3/MLKL signal proteins were detected in cells of each group. Results Compared to those in the control group, the cell viability and the relative expression of BCL-2 in DEX group decreased (P<0.05), the apoptosis rate, ROS relative level, LDH and IL-1β, TNF-α, IL-6 releases, and the relative expressions of BAX and RIP1, RIP3, MLKL proteins increased (P<0.05). Compared to those in DEX group, the cell viability and the relative expression of BCL-2 in DEX+picroside II group increased (P<0.05), the apoptosis rate, ROS relative level, LDH and IL-1β, TNF-α, IL-6 releases, and the relative expressions of BAX and RIP1, RIP3, MLKL proteins decreased (P<0.05). The cell viability and the relative expression of BCL-2 in the DEX+RIP1 overexpression group decreased (P<0.05), the apoptosis rate, ROS relative level, LDH and IL-1β, TNF-α, IL-6 releases, and the relative expressions of BAX and RIP1, RIP3, MLKL proteins increased (P<0.05). There was no obvious difference in cell indexes in DEX+empty plasmid group (P>0.05). Overexpression of RIP1 weakened the effect of picroside II on DEX induced hFOB 1.19 cells. Conclusion Picroside II reduces inflammation by down-regulating RIP1/RIP3/MLKL pathway, thus inhibiting the apoptosis of osteoblasts induced by DEX.
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