红景天苷联合右美托咪定对LPS诱导的人关节软骨细胞凋亡和炎症反应的调节作用  

Synergistic effect and its mechanism of salidroside combined with dexmedetomidine in LPS-induced articular chondrocytes cells

作　　者：杜刚 陈娜 刘晓艳 赵亮[3] Du Gang;Chen Na;Liu Xiaoyan(Dept of Operative Anesthesiology, The First Hospital of Shandong Zibo,Zibo 255200;Dept of Quality Control, The First Hospital of Shandong Zibo,Zibo 255200)

机构地区：[1]山东省淄博市第一医院手术麻醉科,淄博255200 [2]山东省淄博市第一医院质控科,淄博255200 [3]中国人民解放军第960医院淄博分院麻醉科,淄博255300

出　　处：《安徽医科大学学报》2019年第9期1366-1371,共6页Acta Universitatis Medicinalis Anhui

基　　金：山东省自然科学基金(编号:ZR2014HP005)

摘　　要：目的探讨红景天苷(Sal)联合右美托咪定(Dex)对脂多糖(LPS)诱导的人关节软骨细胞凋亡和炎症反应的促进作用和机制。方法分离人关节软骨细胞体系,分别设置健康对照组(Ctrl组)、LPS诱导模型组(LPS组)、单用Sal组(LPS+Sal组)、单用Dex组(LPS+Dex组)、Dex联合Sal组(LPS+Dex+Sal组)。各组模型中LPS刺激8 h(100 ng/ml),Sal(50 μg/ml)和Dex(100 nmol/L)连续作用48 h。免疫荧光检测细胞凋亡;5-溴脱氧尿嘧啶核苷(BrdU)染色鉴定细胞生长状态,Western blot检测软骨细胞凋亡标志分子、细胞功能及通路分子活性;ELISA法检测血清中炎症因子。结果与Ctrl组比较,LPS组细胞发生明显凋亡,凋亡相关标志和通路分子活性明显上调,增殖能力下降,并分泌大量炎症细胞因子( P <0.01)。与LPS组比较,LPS+Sal组与LPS+Dex组细胞凋亡现象有所缓解,凋亡标志及相关通路分子活性下降,增殖能力有所提高,炎症因子分泌水平下降( P <0.01)。与LPS+Dex组比较,LPS+Dex+Sal组细胞凋亡现象显著缓解,并伴随着凋亡标志和通路分子表达水平下调,细胞增殖能力显著提高,炎症因子分泌水平受到明显抑制。结论 Sal可以提高Dex对LPS诱导的人软骨细胞凋亡和炎症反应;其机制可能是通过下调磷酸化核转录因子κB p65(p-NF-κB p65)、肿瘤坏死因子-α(TNF-α)及下游通路活性来发挥作用。Objective To investigate the regulative effect and mechanism of Salidroside(Sal) combined with dexmedetomidine in lipopolysaccharide(LPS)-induced articular chondrocytes cells. Methods The experiment was set as healthy control group(Ctrl group), LPS induction model group(LPS group), Sal group alone(LPS+Sal group), dexmedetomidine(Dex) group alone(LPS+Dex group), Dex combined with Sal group(LPS+Dex+Sal group). In each group, LPS was stimulated for 8 h(100 ng/ml), Sal(50 μg/ml) and Dex(100 nmol/L) for 48 h. For this purpose in this study, the apoptosis were detected by the immunofluorescence;the cells growth were investigated by BrdU staining. The protein expression of apoptosis-and inflammatory-related were determined by Western blot. The levels of inflammatory factors were detected by ELISA. Results The effect of Dex suppressed the apoptosis and inflammation were promoted by Sal in articular chondrocytes cells, inhibited the activation of NF-κB p65, and decreased the inflammatory factors including IL-6, TNF-α and IL-1β, associated with the declined of Caspase-3 and Caspase-9( P <0.01). Conclusion Sal can increase the apoptosis and inflammatory response of Dex induced by LPS in human chondrocytes;the main reason may be by down-regulating phosphorylated nuclear transcriptional κB p65(p-NF-κB p65), tumor necrosis factor-α(TNF-α) and downstream pathway activity.

关 键 词：红景天苷 右美托咪定 关节软骨细胞 凋亡 炎症因子 

分 类 号：R684.3[医药卫生—骨科学]