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蓝萼甲素抑制骨关节炎软骨细胞炎症反应的研究
Inhibitory effect of Glaucocalyxin A on inflammatory response in osteoarthritis chondrocytes
投稿时间:2022-07-15  
DOI:10.3969/j.issn.1672-5972.2023.01.004
中文关键词:  蓝萼甲素  骨关节炎  软骨细胞
英文关键词:Glaucocalyxin A  Osteoarthritis  Chondrocyte
基金项目:陕西省核工业二一五医院院级科研基金项目(215KYJJ-202019)
作者单位邮编
朱伟东* 陕西省核工业二一五医院骨科陕西 咸阳712000 712000
刘岗 陕西省核工业二一五医院骨科陕西 咸阳712000 712000
费国策 陕西省核工业二一五医院骨科陕西 咸阳712000 712000
张勇鹏 陕西省核工业二一五医院骨科陕西 咸阳712000 712000
张博 陕西省核工业二一五医院骨科陕西 咸阳712000 712000
方毅 陕西省核工业二一五医院骨科陕西 咸阳712000 712000
顾世勤 陕西省核工业二一五医院骨科陕西 咸阳712000 712000
许立新 陕西省核工业二一五医院骨科陕西 咸阳712000 712000
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中文摘要:
      目的 探究蓝萼甲素(GLA)对骨关节炎(OA)软骨细胞的影响。方法 根据体外炎症细胞模型构建GLA的不同应用浓度,将人原代关节炎软骨细胞分为以下5组:正常对照组,不对细胞施加任何处理;炎症模型组,即10 ng/mL白细胞介素-1β(IL-1β)处理软骨细胞24 h;梯度浓度GLA(5、10、20 μM)+IL-1β组,即不同浓度(5、10、20 μM)GLA处理软骨细胞2 h,然后用10 ng/mL的IL-1β处理24 h。采用qRT-PCR、Western blot、ELISA检测各组炎症相关分子mRNA和蛋白的表达;采用Western blot、免疫荧光检测各组NF-κB信号通路蛋白的表达。结果 GLA能抑制IL-1β诱导的软骨细胞中诱导型一氧化氮合酶(iNOS)和环氧化酶-2(COX-2)的表达,减少一氧化氮(NO)和前列腺E2(PGE2)的释放;同时,GLA也抑制了IL-1β诱导的软骨细胞中炎性细胞因子TNF-α、IL-6和IL-8的表达;并且,GLA还抑制了软骨细胞中p-p65的表达和p65的核转位,差异均具有统计学意义(P<0.05)。结论 GLA能够减轻骨关节炎软骨细胞的炎症反应,这提示GLA可能成为一种治疗OA的有效药物。
英文摘要:
      Objective To investigate the influence of Glaucocalyxin A (GLA), a natural biological compound, on osteoarthritis (OA) chondrocytes.Methods Primary human osteoarthritis chondrocytes were divided into 5 groups according to the establishment of inflammatory cell model in vitro and different application concentrations of GLA: Normal control group, in which no treatment was applied to the cells; inflammatory model group, in which chondrocytes were treated with 10 ng/mL interleukin-1β (IL-1β) for 24 h; gradient concentration of GLA (5, 10, 20 μM) + IL-1β groups, in which chondrocytes were treated with different concentrations (5, 10, 20 μM) of GLA for 2 h, and then treated with 10 ng/mL IL-1β for 24 h. The mRNA and protein expression of inflammation related factors was detected by qRT-PCR, Western blot and ELISA. The NF-κB signal pathway protein expression was detected by Western blot and immunofluorescence in each group.Results GLA could inhibit the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in chondrocytes induced by IL-1β, and reduce the release of nitric oxide (NO) and prostaglandin E2 (PGE2). At the same time, GLA could also inhibit the production of inflammatory cytokines such as TNF-α, IL-6 and IL-8 in chondrocytes induced by IL-1β. GLA also inhibited the expression of p-p65 and the nuclear translocation of p65 in chondrocytes, and the differences were statistically significant (all P<0.05).Conclusion GLA can alleviate the inflammatory response of OA chondrocytes, which suggests that GLA may be an effective drug for the treatment of OA.
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