首页|蛇床子素通过NF-kB信号通路调控退变髓核细胞的细胞外基质表达、炎症反应及凋亡

蛇床子素通过NF-kB信号通路调控退变髓核细胞的细胞外基质表达、炎症反应及凋亡

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目的 研究蛇床子素对退变髓核细胞的细胞外基质表达、炎症反应和凋亡的作用及其潜在机制。方法 采用氧糖剥夺(Oxygen Glucose Deprivation,OGD)培养建立退变髓核细胞模型,将细胞分为:对照组(正常培养)、OGD组(OGD培养)、蛇床子素组(OGD培养+蛇床子素处理)、PDTC组(OGD培养+NF-KB通路抑制剂PDTC处理)和蛇床子素+PDTC组(OGD培养+蛇床子素+PDTC处理)。采用Western blot检测细胞中Ⅱ型胶原(Collagen type Ⅱ,Col2al)、聚集蛋白聚糖(Aggrecan)、P65和p-P65蛋白表达,ELISA法检测细胞培养液中炎性因子血清白细胞介素-1 β(interleukin-1β,IL-1β),白细胞介素-6(interleukin-6,IL-6)和肿瘤坏死因子-α(Tumor necrosis factor-α,TNF-α)的水平,流式细胞仪检测细胞凋亡率。结果 与对照组比较,OGD组细胞中Col2al、Aggrecan蛋白相对表达水平明显降低,细胞培养液中IL-1β、IL-6和TNF-α水平升高,细胞凋亡率明显升高,细胞中p-P65蛋白表达明显升高;与OGD组比较,蛇床子素组和PDTC组细胞中Col2al、Aggrecan蛋白相对表达水平明显升高,细胞培养液中IL-1β、IL-6和TNF-α水平降低,细胞凋亡率明显降低,细胞中p-P65蛋白表达明显降低,而蛇床子素+PDTC组上述指标改变最为明显。结论 蛇床子素可能通过抑制核因子激活的B细胞的κ轻链增强(nuclear factor κB,NF-κB)信号通路的活性,促进退变髓核细胞的细胞外基质合成、抑制退变髓核细胞的炎症反应和凋亡。
Osthole Regulates Extracellular Matrix Expression,Inflammatory Response and Apoptosis of Degenerative Nucleus Pulposus Cells Through NF-KB Signaling Pathway
Objective To investigate the effect of osthole on extracellular matrix expression,inflammatory response and apopto-sis of degenerative nucleus pulposus cells and its potential mechanism.Methods The degraded nucleus pulposus cell model was established by oxygen glucose deprivation(OGD)culture,and the cells were divided into control group(normal culture),OGD group(OGD culture),osthole group(OGD culture+osthole treatment),PDTC group(OGD culture+NF-KB pathway inhibitor PDTC treatment)and osthole+PDTC group(OGD culture+osthole+PDTC treatment).The expressions of collagen type II(Col2al),Aggrecan,P65 and P-P65 proteins in the cells were detected by Western blot,the levels of inflammatory cytokines in-terleukin-1β(IL-1β),interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)in the cell culture medium were de-tected by ELISA,and the apoptosis rate was detected by flow cytometry.Results Compared with those of the control group,the rel-ative expressions of Col2al and Aggrecan proteins in the OGD group were significantly decreased,the levels of IL-1,IL-6 and TNF-α in the cell culture medium were increased,the apoptosis rate was significantly increased,and the expression of P-P65 protein was significantly increased.Compared with those of the OGD group,the relative expression levels of Col2al and Aggrecan proteins in the cells of the osthole group and the PDTC group were significantly increased,the levels of IL-1 β,IL-6 and TNF-α in the cell culture medium were significantly decreased,the apoptosis rate was significantly decreased,and the expression of P-P65 protein in the cells was significantly decreased,while the changes of the above indicators in the osthole+PDTC group were the most obvious.Conclusions Osthole may inhibit the extracellular matrix degradation,inflammatory response and apoptosis of degenerative nucleus pulposus cells by inhibiting the activity of NF-kB signaling pathway.

nucleus pulposus cellsostholeNF-kB signaling pathwayextracellular matrixinflammatoryapoptosis

高峰、于喜微、李晨辰

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锦州医科大学附属第三医院,辽宁锦州 121000

髓核细胞 蛇床子素 NF-kB信号通路 细胞外基质 炎症反应 凋亡

国家中医药局科研项目辽宁省教育厅科研项目

2020XZ5029JYTYLXY202006

2024

中华中医药学刊
中华中医药学会 ,辽宁中医药大学

中华中医药学刊

CSTPCD北大核心
影响因子:1.007
ISSN:1673-7717
年,卷(期):2024.42(3)
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