金丝桃苷对IL⁃1β诱导的小鼠骶髂关节软骨细胞损伤的影响  被引量:4

Effects of hyperin on sacroiliac joint of mice with IL⁃1β⁃induced chondrocyte injury

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作  者:王西彬 左瑞庭 WANG Xi-bin;ZUO Rui-ting(Department of Spine Care,Henan Provincial Hospital of TCM(The Second Hospital Affiliated to Henan University of Chinese Medicine),Zhengzhou 450002,China;Department of Rheumatology,Henan Provincial Hospital of TCM(The Second Hospital Affiliated to Henan University of Chinese Medicine),Zhengzhou 450002,China)

机构地区:[1]河南省中医院(河南中医药大学第二附属医院)脊柱科,河南郑州450002 [2]河南省中医院(河南中医药大学第二附属医院)风湿科,河南郑州450002

出  处:《中成药》2021年第2期369-373,共5页Chinese Traditional Patent Medicine

摘  要:目的探讨金丝桃苷对IL⁃1β诱导的小鼠骶髂关节软骨细胞活性、炎性因子水平、细胞外基质(ECM)平衡,以及核因子NF⁃κB信号通路的影响。方法分离培养BALB/c小鼠骶髂关节软骨细胞,并将其随机分成5组,对照组、IL⁃1β组、IL⁃1β+金丝桃苷(25、50、100μg/mL)组。MTT检测细胞活性;ELISA试剂盒检测白介素(IL)⁃6、肿瘤坏死因子(TNF)⁃α、Ⅰ型胶原(Col⁃Ⅰ)和Ⅲ型胶原(Col⁃Ⅲ)水平;Western blot检测基质金属蛋白酶(MMP)⁃3、MMP⁃9、p⁃IκB⁃α和p⁃p65的表达。结果IL⁃1β处理显著抑制软骨细胞活性,提高IL⁃6和TNF⁃α水平,降低Col⁃Ⅰ和Col⁃Ⅲ的水平,并上调MMP⁃3、MMP⁃9、p⁃IκB⁃α和p⁃p65的表达;而金丝桃苷呈浓度依赖性抑制IL⁃1β诱导的细胞活性下降,IL⁃6和TNF⁃α水平上升,Col⁃Ⅰ和Col⁃Ⅲ水平下降,以及MMP⁃3、MMP⁃9、p⁃IκB⁃α和p⁃p65的表达上调。结论金丝桃苷能够抵抗IL⁃1β诱导的小鼠骶髂关节软骨细胞损伤,提高细胞活性、抑制炎性因子和ECM紊乱,这与其抑制NF⁃κB信号通路有关。AIM To investigate the effects of hyperin on the chondrocyte viability,inflammatory factor level,extracellular matrix(ECM)balance,and NF⁃κB signaling pathway of mice sacroiliac joint with IL⁃1β⁃induced injury.METHODS The isolated BALB/c mice sacroiliac joint chondrocytes were randomly divided into 5 groups as control group,IL⁃1βgroup,IL⁃1β+hyperin groups(25,50,100μg/mL).The cells were subjected to the detection of cell viability by MTT;the determination of levels of interleukin(IL)⁃6,tumor necrosis factor(TNF)⁃α,type I collagen(Col⁃Ⅰ)and typeⅢcollagen(Col⁃Ⅲ)by ELISA kits;and the identification of expression of matrix metalloproteinase(MMP)⁃3,MMP⁃9,p⁃IκB⁃αand p⁃p65 by Western blotting.RESULTS The significant inhibition of chondrocyte viability,increase in levels of IL⁃6 and TNF⁃α,decrease in levels of Col⁃Ⅰand Col⁃Ⅲ,and up⁃regulation of expression of MMP⁃3,MMP⁃9,p⁃IκB⁃αand p⁃p65 due to IL⁃1βtreatment were offset by hyperin in a concentration⁃dependent manner.CONCLUSION Hyperin counteracts the effect of IL⁃1βin chondrocyte injury induction of mouse sacroiliac joint,in terms of cell viability increase,and inhibition of inflammatory factors and ECM disorders via inactivation of NF⁃κB signaling pathway.

关 键 词:金丝桃苷 软骨细胞 炎性因子 细胞外基质 NF⁃κB信号通路 

分 类 号:R285.5[医药卫生—中药学]

 

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