摘要
目的:观察小檗碱联合人参皂苷Rb1对脂肪细胞炎症信号通路的影响。方法:将诱导分化成熟的3T3-L1脂肪细胞分在肿瘤坏死因子(TNF-α)作用下给予小檗碱、人参皂苷Rb1、小檗碱和人参皂苷Rb1合用处理后,观察药物对脂肪细胞炎症信号通路的作用。结果:基础状态下,与空白对照组相比,Ber组脂肪细胞的TNF-α和IL-6的mRNA表达量降低更明显(P<0.01)。胰岛素抵抗(TNF-α刺激)状态下,与空白对照组比较,Ber组能显著地抑制TNF-α刺激下上调的TNF-α、IL-6的表达(P<0.01),而Rb1仅抑制TNF-α的表达(P<0.01),Ber+Rb1两药合用,与Rb1单用作用类似,仅抑制了TNF-α的表达(P<0.01)。经TNF-α诱导后,加入Ber处理的脂肪细胞,NF-κB和IKK-β表达水平下调,而加入Rb1处理的脂肪细胞(无论是否+Ber),NF-κB和IKK-β表达水平上调。结论:小檗碱和人参皂苷Rb1两者合用对脂肪炎性细胞未能显示出增效作用。
Objective:To observe the effects of ginsenoside Rb1 and its combination with berberine on inflammatory signaling pathways in adipocytes.Methods:The differentiated 3 T3-L1 adipocytes were stimulated with tumor necrosis factor-α(TNF-α),treated with berberine,ginsenosides Rb1,and both berberine and ginsenosides Rb1.The effect of drugs on inflammatory signal pathway of adipocytes was observed.Results:In the basal state,compared with the blank control group,the mRNA expression of TNF-αand IL-6 in the adipocytes of the Ber group decreased more significantly(P<0.01).In the insulin resistance(TNF-αstimulation)state,compared with the blank control group,the Ber group could significantly inhibit the up-regulated expression of TNF-αand IL-6 under the stimulation of TNF-α(P<0.01),while Rb1 only inhibited the expression of TNF-α(P<0.01).The combination of Ber and Rb1,similar to Rb1 alone,only inhibited the expression of TNF-α(P<0.01).After TNF-αinduction,the expression levels of NF-κB and IKK-βwere down regulated in the adipocytes treated with Ber,while the expression levels of NF-κB and IKK-βwere up regulated in the adipocytes treated with Rb1(whether or not+Ber).Conclusions:Berberine combined with ginsenoside Rb1 did not show synergistic effect on adipoinflammatory cells.
作者
蔡之幸
陈越
CAI Zhixing;CHEN Yue(Department of Traditional Chinese Medicine,Tongren Hospital Affiliated to Shanghai Jiaotong University School of Medicine,Shanghai 200336)
出处
《陕西中医》
2020年第3期297-300,共4页
Shaanxi Journal of Traditional Chinese Medicine
基金
国家自然科学基金资助横向合作课题(TR2017T02)
同仁医院院级课题(TRYJ201707),同仁医院一般学科建设项目(2017XK32).
作者简介
通讯作者:陈越
