生骨再造丸抑制TNF-α调控程序性坏死RIP1/RIP3-MLKL信号通路对MLO-Y4骨样细胞的作用机制
The mechanism of inhibition of TNF-alpha-regulated programmed necrosis RIP1/RIP3-MLKL signaling pathway by Shenggu Zaizao Pill (SGZZP) in MLO-Y4 bone-like cells
  
DOI:10.3969/j.issn.1006-7108.2026.09.003
中文关键词:  生骨再造丸  TNF-α  程序性坏死  骨质疏松症  MLO-Y4细胞  含药血清
英文关键词:SGZZP  TNF-α  programmed necrosis  osteoporosis  MLO-Y4 cells  drug-containing serum
基金项目:国家自然科学基金(82460941);甘肃省自然科学基金(24JRRA549);甘肃省中医药管理局项目(GZKP-2022-20);张晓刚全国名老中医药专家传承工作室建设项目(国中医药人教函〔2022〕75号);兰州市科技局计划项目(2023-2-7);甘肃省卫生健康行业科研项目(GSWSQN2023-10)
作者单位
李纪书1 刘志寰1 张喆1 郭成龙2* 张晓刚2 刘凯雯1 寇文洁1 1.甘肃中医药大学,甘肃 兰州 730000 2.甘肃中医药大学附属医院,甘肃 兰州 730000 
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中文摘要:
      目的 探讨生骨再造丸抑制肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)调控程序性坏死对MLO-Y4骨样细胞的作用及机制研究。方法 采用CCK8实验检测筛选出生骨再造丸含药血清(10%、20%、40%、60%、100%)作用于TNF-α诱导MLO-Y4细胞增殖最佳浓度;采用CCK8实验检测生骨再造丸含药血清最佳浓度在不同干预条件下MLO-Y4细胞体外增殖能力的影响;采用流式细胞术检测MLO-Y4骨样细胞在各种条件干预下,细胞凋亡情况及对比;采用实时荧光定量聚合酶链式反应(quantitativereal-time PCR,qRT-PCR)检测程序性坏死相关RIP1、RIP3、MLKL、Caspase8 mRNA;采用蛋白免疫印迹法检测MLO-Y4细胞中程序性坏死相关蛋白RIP1、RIP3、MLKL、Caspase8。结果 与空白组比较,生骨再造丸组给药浓度40%时促进MLO-Y4细胞增殖率最明显;与模型组相比较,生骨再造丸干预组具有促进MLO-Y4细胞增殖作用;与模型组相比较,生骨再造丸干预组具有抑制MLO-Y4细胞凋亡作用;与空白组相比较TNF-α具有促进RIP1、RIP3、MLKL、Caspase8 mRNA表达的作用;与模型组相比较生骨再造丸具有抑制RIP1、RIP3、MLKL、Caspase8蛋白表达作用。结论 生骨再造丸可能通过抑制TNF-α表达,进而调控RIP1/RIP3-MLKL信号通路轴,通过抑制TNF-α调控程序性坏死RIP1/RIP3-MLKL信号通路,使细胞内的RIP1、RIP3、MLKL下降,进而促进MLO-Y4细胞增殖。
英文摘要:
      Objective To study the effect and mechanism of Shenggu Zaizao Pill (SGZZP) on MLO-Y4 osteoid cells by inhibiting TNF-α-regulated programmed necrosis. Methods CCK8 assay was used to detect and select the optimal concentration of serum containing SGZZP (10%, 20%, 40%, 60%, 100%) for TNF-α-induced MLO-Y4 cell proliferation in vitro. The effect of the optimal concentration of SGZZP on the proliferation of MLO-Y4 cells in vitro under different intervention conditions was detected with CCK8 assay. Flow cytometry was used to detect the apoptosis of MLO-Y4 osteoid cells under various conditions. The mRNA of RIP1, RIP3, MLKL and Caspase 8 associated with programmed necrosis was detected with real-time quantitative PCR. The protein levels of RIP1, RIP3, MLKL, and Caspase 8 associated with programmed necrosis in MLO-Y4 cells were detected with Western blotting. Results Compared to the the blank group, SGZZP group promoted the proliferation rate of MLO-Y4 cells most obviously when the dose concentration was 40%. Compared to the model group, SGZZP promoted the proliferation of MLO-Y4 cells, and inhibited the apoptosis of MLO-Y4 cells. Compared to the blank group, TNF-α promoted mRNA levels of RIP1, RIP3, MLKL, and Caspase 8. Compared to the model group, SGZZP inhibited the protein expressions of RIP1, RIP3, MLKL, and Caspase 8. Conclusion SGZZP may regulate the axis of RIP1/RIP3-MLKL signaling pathway by inhibiting the expression of TNF-α. It regulates the programmed necrosis RIP1/RIP3-MLKL signaling pathway by inhibiting TNF-α, thereby reducing the intracellular RIP1, RIP3, and MLKL and promoting the proliferation of MLO-Y4 cells.
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