红景天苷对关节软骨细胞炎性损伤的影响  

Impacts of salidroside on inflammatory injury of articular chondrocytes

作　　者：张学登 先明博 王红辉[1] ZHANG Xuedeng;XIAN Mingbo;WANG Honghui(Nanyang Medical College First Affiliated Hospital Orthopedics Second Ward,Nanyang 473000,China)

机构地区：[1]南阳医学高等专科学校第一附属医院骨科二病区,河南南阳473000

出　　处：《中国骨质疏松杂志》2024年第12期1781-1786,共6页Chinese Journal of Osteoporosis

摘　　要：目的 探究红景天苷(Sal)对关节软骨细胞炎性损伤的影响。方法 将人关节软骨细胞分为对照组(常规培养)、IL-1β组(50 ng/mL)、Sal-2μmol/L、Sal-4μmol/L、Sal-8μmol/L组,Sal+GW0742组(8μmol/L Sal+4μmol/L CCL2-CCR2信号轴激活剂GW0742)。采用50 ng/mL IL-1β处理人关节软骨细胞以建立关节软骨细胞损伤模型。MTT法检测Sal及GW0742对关节软骨细胞的毒性;平板克隆实验、流式细胞术检测细胞增殖和凋亡;ELISA检测炎症相关因子(IL-10、TNF-α、IL-6)水平;qRT-PCR检测CCL2、CCR2mRNA表达;Western blot检测增殖、凋亡相关蛋白(PCNA、Cleaved Caspase-3)及CCL2-CCR2信号轴蛋白表达。结果 相较于对照组,IL-1β组集落形成数、IL-10、PCNA表达降低,凋亡率、TNF-α、IL-6、CCL2、CCR2mRNA及Cleaved Caspase-3、CCL2、CCR2表达升高(P<0.05);相较于IL-1β组,Sal-2μmol/L、Sal-4μmol/L、Sal-8μmol/L组集落形成数、IL-10、PCNA表达依次升高,凋亡率、TNF-α、IL-6、CCL2、CCR2mRNA及Cleaved Caspase-3、CCL2、CCR2表达依次降低(P<0.05);CCL2-CCR2信号通路激活剂GW0742可减弱Sal对IL-1β诱导的关节软骨细胞炎性损伤的保护作用(P<0.05)。结论 Sal可能通过抑制CCL2-CCR2通路,从而抑制IL-1β诱导的关节软骨细胞凋亡和炎症反应。Objective To investigate the impacts of salidroside(Sal)on inflammatory injury of articular chondrocytes.Methods Experimental group:Human articular chondrocytes were separated into control group(conventional culture),IL-1βgroup(50 ng/mL),Sal-2μmol/L,Sal-4μmol/L,Sal-8μmol/L groups,and Sal+GW0742 group(8μmol/L Sal+4μmol/L CCL2-CCR2 signal axis activator GW0742).Human articular chondrocytes were treated with 50ng/mL IL-1βto establish the injury model of articular chondrocytes.MTT method was applied to detect the toxicity of Sal and GW0742 on articular chondrocytes.Plate cloning experiments and flow cytometry were applied to detect cell proliferation and apoptosis.ELISA was applied to detect the levels of inflammation related factors(IL-10,TNF-α,IL-6).QRT-PCR was applied to detect the expression of CCL2 and CCR2 mRNA in cells.Western blot was applied to detect the expression of proliferation and apoptosis related proteins(PCNA,Cleaved Caspase-3)and CCL2-CCR2 signaling axis proteins.Results Compared to the control group,the number of colony formation,the expression of IL-10,and PCNA reduced in the IL-1βgroup,the apoptosis rate,the expression of TNF-α,IL-6,CCL2,CCR2 mRNA,and the expression of Cleaved Caspase-3,CCL2,and CCR2 increased(P<0.05).Compared to the IL-1βgroup,the number of colony formation,the expression of IL-10,and PCNA in the Sal-2μmol/L,Sal-4μmol/L,and Sal-8μmol/L groups increased sequentially,the apoptosis rate,the expression of TNF-α,IL-6,CCL2,CCR2 mRNA,and the expression of Cleaved Caspase-3,CCL2,and CCR2 decreased sequentially(P<0.05).CCL2-CCR2 signaling pathway activator GW0742 was able to weaken the protective effect of Sal on IL-1β-induced inflammatory injury of articular chondrocytes(P<0.05).Conclusion Sal may inhibit IL-1β-induced apoptosis and inflammatory response of articular chondrocytes by inhibiting the CCL2-CCR2 pathway.

关 键 词：红景天苷 CCL2-CCR2信号轴 关节软骨细胞 炎症 凋亡 

分 类 号：R285.5[医药卫生—中药学]