依泽替米贝通过小凹蛋白1调节大鼠血管平滑肌细胞内脂质蓄积

目的:观察依泽替米贝(ezeti mibe)对大鼠血管平滑肌细胞内胆固醇蓄积的影响以及相关的作用机制。方法:以原代培养大鼠血管平滑肌细胞(rat VSMCs)为研究对象,以20 mg/L胆固醇:甲基β环糊精复合物(Chol:MβCD)孵育细胞48 h形成荷脂细胞模型。不同浓度的依泽替米贝(3、10、30μmol/L)处理细胞24 h,或以30μmol/L依泽替米贝分别处理细胞不同时间(0、6、12、24、48 h),HPLC检测细胞内TC、游离胆固醇(FC)的含量,Western blotting检测小凹蛋白1(caveolin-1)蛋白的表达。结果:不同浓度依泽替米贝(3、10、30μmol/L)作用于VSMCs源性荷脂细胞不同时间,细胞内TC、FC的含量呈浓度依赖性减少,以30μmol/L浓度孵育24 h作用最强。Chol:MβCD明显减少细胞caveolin-1蛋白表达水平,依泽替米贝能够逆转这种作用。结论:依泽替米贝抑制Chol:MβCD诱导的大鼠平滑肌细胞中胆固醇蓄积作用可能与caveolin-1有关。     

载脂蛋白嵌合模拟肽对低密度脂蛋白诱导的巨噬细胞凋亡的影响

目的观察模拟肽Ac-hE-18A-NH2对氧化低密度脂蛋白(oxLDL)诱导的RAW264.7巨噬细胞凋亡的影响。方法50 mg.L-1oxLDL处理RAW 264.7细胞48 h后加入不同浓度的Ac-hE-18A-NH2(1、10、50、100 mg.L-1)和β-环糊精(β-CD)或布雷菲得菌素(BFA)共同孵育24 h。通过流式细胞仪检测细胞凋亡,试剂盒检测caspase-3活性及细胞内胆固醇含量,Western blot检测细胞bcl-2蛋白的表达,液体闪烁计数器检测细胞内胆固醇流出。结果 oxLDL诱导的RAW 264.7巨噬细胞的凋亡率随着oxLDL浓度的增加和处理时间的延长而明显提高。Ac-hE-18A-NH2(1、10、50、100mg.L-1)干预后细胞凋亡率以浓度依赖的方式减少。Ac-hE-18A-NH2呈浓度依赖性的促进细胞内胆固醇流出和降低细胞内的胆固醇含量,降低caspase-3的活性,上调bcl-2的蛋白表达。β-CD与Ac-hE-18A-NH2共同作用后胆固醇流出明显增加,细胞凋亡率相应减少。而BFA作用相反。结论Ac-hE-18A-NH2明显抑制oxLDL诱导的巨噬细胞凋亡,其作用可能与促进细胞胆固醇流出、减少细胞内胆固醇蓄积有关。     

脂联素对巨噬细胞源性泡沫细胞ABCA1及胆固醇含量的影响及机制

目的探讨脂联素对RAW264.7巨噬细胞源性泡沫细胞ABCA1及胆固醇含量的影响及其可能的机制。方法体外培养RAW264.7细胞,加入20 mg/L氧化低密度脂蛋白(ox-LDL)共同孵育48 h,将其诱导成泡沫细胞,加入不同浓度(0、1、5、10μg/mL)的脂联素干预24 h,RT-PCR测定ABCA1 mRNA的表达,高效液相色谱测定细胞内胆固醇含量。观察脂联素对泡沫细胞中ABCA1表达的影响。结果脂联素显著增加RAW264.7巨噬细胞源性泡沫细胞ABCA1 mRNA的表达(P<0.05),并增加细胞内胆固醇含量,且呈浓度依赖性(P<0.05)。结论脂联素可以增加巨噬源性泡沫细胞ABCA1转录水平,促进胆固醇流出,延缓AS的发生发展。     

PPARγ激动剂对RAW264.7巨噬细胞源性泡沫细胞胆固醇流出的影响

目的观察PPARγ激动剂吡格列酮对RAW264.7巨噬细胞源性泡沫细胞胆固醇流出调节蛋白三磷酸腺苷结合核转运蛋白G1(ABCG1)、肝X受体α(LXRα)表达的影响。方法 (1)体外培养RAW 264.7巨噬细胞,用50 mg/L的氧化型低密度脂蛋白胆固醇(ox-LDL)孵育48 h诱导成泡沫细胞,油红O染色并在光镜下鉴定泡沫细胞形态及变化。(2)以不同浓度吡格列酮(0、5、10、20、30μmol/L)作用泡沫细胞24 h后,酶法检测泡沫细胞内胆固醇酯的含量。用反转录-聚合酶链反应(RT-PCR)及免疫印迹法测定ABCG1、LXRα的mRNA及蛋白的表达。结果 PPARγ激动剂吡格列酮可显著减少泡沫细胞内胆固醇酯含量,并呈浓度依赖性增加RAW264.7巨噬细胞源性泡沫细胞ABCG1、LXRα的mRNA和蛋白的表达。结论 PPARγ激动剂吡格列酮减少泡沫细胞内胆固醇酯的含量可能是通过上ABCG1、LXRα的mRNA及蛋白表达来实现的。     

八肽胆囊收缩素通过p38MAPK通路抑制LPS诱导的RAW264.7细胞IL-1β表达

目的研究八肽胆囊收缩素(CCK-8)对LPS诱导RAW264.7细胞IL-1β表达的影响及相关机制。方法用ELISA及RT-PCR法检测RAW264.7细胞IL-1βmRNA及蛋白表达;用Western blot检测RAW264.7细胞p38 MAPK的磷酸化水平。结果①LPS可时间依赖性的诱导RAW264.7细胞IL-1βmRNA及蛋白的表达,分别于刺激后3 h及6 h达到高峰;②10-10 mol.L-1 CCK-8对LPS诱导的RAW264.7细胞IL-1β表达无影响;10-8、10-6 mol.L-1CCK-8浓度依赖性地抑制了LPS诱导的RAW264.7细胞IL-1β表达;③10-10 mol.L-1 CCK-8未影响LPS诱导的p-p38MAPK水平,10-8、10-6 mol.L-1 CCK-8浓度依赖性地抑制了LPS诱导的p-p38 MAPK水平;④p38 MAPK特异性抑制剂SB203580可抑制LPS诱导的RAW264.7细胞IL-1β表达,与CCK-8共同作用后,抑制作用进一步加强。结论 CCK-8通过抑制p38 MAPK磷酸化而抑制了LPS诱导的RAW264.7细胞IL-1β表达,这可能是CCK-8发挥抗炎作用的信号转导机制之一。     

八肽胆囊收缩素抑制LPS诱导的RAW264.7细胞AP-1活性及IL-6表达

目的研究八肽胆囊收缩素(CCK-8)对LPS诱导RAW264.7细胞IL-6表达的影响及相关机制。方法用ELISA及RT-PCR法检测RAW264.7细胞IL-6蛋白及mR-NA表达;用EMSA方法检测RAW264.7细胞AP-1 DNA结合活性。结果①LPS可时间依赖性的诱导RAW264.7细胞IL-6蛋白及mRNA表达;②10-10 mol.L-1 CCK-8对LPS诱导的RAW264.7细胞IL-6表达无明显影响;10-8、10-6 mol.L-1 CCK-8浓度依赖性地抑制了LPS诱导的RAW264.7细胞IL-6表达;③10-10 mol.L-1 CCK-8未影响LPS诱导的AP-1活性,10-8、10-6 mol.L-1 CCK-8浓度依赖性地抑制了LPS诱导的AP-1活性。结论 CCK-8通过抑制AP-1 DNA结合活性而抑制了LPS诱导的RAW264.7细胞IL-6表达,这可能是CCK-8发挥抗炎作用的信号转导机制之一。     

儿茶素对Caco-2细胞胆固醇摄取的影响及机制研究

目的： 研究儿茶素（Catechin，Cat）对Caco-2细胞胆固醇摄取的影响，以及可能的作用机制。方法： 利用胆固醇：甲基β环糊精复合物（Chol：MβCD）建立Caco-2细胞脂质蓄积模型。不同浓度的儿茶素（20、40、60 μmol·L^-1）处理细胞24 h，结合油红O染色法观察细胞内的脂质蓄积，酶法测定细胞内胆固醇含量及分布，qRT-PCR及Westernblot检测胆固醇代谢相关基因NPC1L1和SREBP-2的表达。结果： 与空白组相比，Chol：MβCD处理组细胞内红色脂滴颗粒以及胆固醇含量明显增加。20~60 μmol·L^-1儿茶素不仅可以不同程度地减少细胞内红染脂滴的形成，而且可以显著降低细胞内总胆固醇和游离胆固醇的含量，以及胆固醇酯在总胆固醇中的比例。此外，儿茶素可以剂量依赖性地降低胆固醇代谢相关基因NPC1L1及SREBP-2的mRNA和蛋白表达。其中以60 μmol·L^-1 Cat处理组的作用最为显著（P<0.01）。结论： 儿茶素可能通过下调胆固醇代谢相关基因NPC1L1和SREBP-2的表达，进而减少Caco-2细胞摄取胆固醇及蓄积。     

神经前体细胞表达下调因子8类泛素修饰抑制因子MLN4924对单核巨噬细胞白血病细胞增殖和凋亡的影响

目的观察神经前体细胞表达下调因子8(NEDD8)类泛素修饰抑制因子MLN4924对单核巨噬细胞白血病细胞增殖的影响,并探讨其作用机制。方法 MLN4924 0.25~4.0μmol·L-1与U937细胞、THP-1细胞、Mo7e细胞和RAW264.7细胞作用24 h,采用MTT法检测细胞存活。MLN4924 0.25~8.0μmol·L-1与RAW264.7细胞作用24 h,用Western蛋白质印迹法检测NEDD8类泛素化修饰的主要底物cullin蛋白表达水平。MLN4924 0.5μmol·L-1作用于RAW264.7细胞24 h,用流式细胞仪检测细胞周期和细胞凋亡率。结果 MLN4924 0.25~4.0μmol·L-1作用24 h对RAW264.7细胞、U937细胞、THP-1细胞和Mo7e细胞增殖具有抑制作用,IC50分别为0.52,3.11,2.89和0.76μmol·L-1;对正常小鼠骨髓巨噬细胞增殖无明显影响。MLN4924 0.25~8.0μmol·L-1作用24 h,NEDD8类泛素化修饰的cullin蛋白表达减少(P<0.01),表明RAW264.7细胞NEDD8修饰逐渐减少。MLN4924 0.5,1.0和2.0μmol·L-1作用于RAW264.7细胞24 h,G0/G1期细胞百分率由正常对照组的(61.3±1.3)%分别升高到(64.5±1.5)%(P<0.05),(69.5±2.3)%(P<0.01)和(72.8±1.7)%(P<0.01),细胞凋亡率由正常对照组的(1.5±0.3)%分别升高到(2.3±0.5)%,(4.3±0.9)%(P<0.05)和(7.5±0.8)%(P<0.01)。结论 MLN4924能够明显抑制单核巨噬细胞白血病细胞增殖,并诱导其细胞周期阻滞和细胞凋亡。     

番茄红素对巨噬细胞源性荷脂细胞胆固醇代谢及其相关蛋白Srebp-1、Caveolin-1表达的影响

目的:研究番茄红素对巨噬细胞源性荷脂细胞胆固醇代谢及其相关蛋白固醇调节元件结合蛋白1(Srebp-1)、小凹蛋白1(Caveolin-1)表达的影响。方法:建立巨噬细胞源性荷脂细胞模型,采用高效液相色谱法考察不同浓度(12.5、25、50μmol/L)番茄红素作用于荷脂细胞24h及25μmol/L番茄红素作用于荷脂细胞不同时间(12、24、48、72h)后细胞内总胆固醇(TC)、游离胆固醇(FC)和胆固醇酯(CE)的含量;蛋白印迹法检测番茄红素(25μmol/L、24h)组及其与Srebp-1蛋白抑制剂ALLN(20μmol/L、24h)联用组对荷脂细胞中Srebp-1、Caveolin-1蛋白表达的影响。另设立正常巨噬细胞组和荷脂细胞组进行比较。结果:与正常巨噬细胞组比较,荷脂细胞组细胞内TC、FC、CE含量均明显升高,Srebp-1、Caveolin-1蛋白表达明显减弱(P<0.05);与荷脂细胞组比较,番茄红素组荷脂细胞内TC、FC、CE含量均明显降低且呈一定的浓度和时间依赖性,Srebp-1、Caveolin-1蛋白表达明显增强(P<0.05);与番茄红素组比较,联用组细胞内Srebp-1、Caveolin-1蛋白表达均明显减弱(P<0.05)。结论:番茄红素能引起巨噬细胞源性荷脂细胞内TC、FC、CE含量降低,且可能与Srebp-1及Caveolin-1蛋白的表达上调有一定关系。     

新型降脂药依泽替米贝的研究进展

依泽替米贝是先灵普劳公司与默克公司共同研制开发的一种新型的降脂药,美国FDA于2002年批准上市。它作用于小肠刷状缘的NPC1L1、膜联蛋白2小凹蛋白1、氨肽酶N等蛋白质,起着抑制胆固醇吸收的作用。它的作用机制与他汀类药物互补,后者可以抑制体内胆固醇合成。临床试验表明,依泽替米贝无论是单用还是与他汀类联合应用,都能收到很好的降脂效果,并且降脂的同时能降低低密度脂蛋白胆固醇水平,升高高密度脂蛋白胆固醇水平。另外,依泽替米贝对一些难治性的遗传性高胆固醇血症如家族型纯合子高脂血症有很好的疗效。     

芦荟大黄素对LPS诱导的RAW264.7细胞NO生成及iNOS表达的影响

目的观察芦荟大黄素(aloe-emodin)对脂多糖(LPS)诱导的RAW264.7细胞一氧化氮(NO)生成及诱生型一氧化氮合酶(iNOS)mRNA表达的作用。方法采用LPS诱导的RAW264.7细胞株建立细胞炎症反应模型。采用Griess试剂法测定NO释放量;采用硝普钠释放NO法测定NO自由基含量的变化;采用反转录聚合酶链反应(RT-PCR)分析iNOS mRNA表达改变。结果芦荟大黄素在0.69～2.50mg·L-1剂量范围内可抑制LPS诱导的RAW264.7细胞NO的释放,并呈剂量和时间依赖关系;芦荟大黄素在0.63～5.00mg·L-1剂量范围内可下调LPS诱导的RAW264.7细胞iNOS mRNA含量;而此范围内芦荟大黄素无直接清除NO自由基作用,不影响iNOS活性。结论芦荟大黄素可明显降低LPS诱导的RAW264.7细胞NO释放,呈时间和剂量依赖关系,此作用并非通过捕捉NO或抑制iNOS活性来实现,而是通过抑制iNOS mRNA表达发挥作用的。     

金丝桃苷对新生大鼠神经细胞缺氧/再给氧损伤的保护作用及其机制

目的探讨金丝桃苷(hyperin,Hyp)对新生大鼠脑细胞缺氧/再给氧损伤的保护作用及其机制。方法将分离的新生大鼠脑细胞缺氧30min或缺氧30min后再给氧40min造成细胞缺氧或再给氧损伤模型,测定细胞培养上清液中乳酸脱氢酶(LDH)、丙二醛(MDA)和一氧化氮(NO)水平的变化,用Fura2-AM方法测定脑细胞内游离钙离子浓度([Ca2+]i)的变化。结果脑细胞缺氧时,细胞培养上清液中LDH从(62.0±13.0)U·L-1(Sham组)增高到(116.0±16.6)U·L-1(Control组,P<0.01),再给氧时,LDH和MDA分别从(45.6±9.2)U·L-1和(9.1±0.9)μmol·L-1(Sham组)增高到(106.0±17.4)U·L-1和(16.4±2.7)μmol·L-1(Control组,P<0.01)。Hyp在1.0～16.0μmol·L-1范围内,明显地抑制缺氧及再给氧损伤诱导的上述LDH和NO增高,并呈一定的浓度依赖性。1.0～16.0μmol·L-1的Hyp不仅可明显地抑制缺氧诱导的细胞培养上清液中NO和脑细胞内[Ca2+]i的增高(P<0.05或P<0.01),也可明显地抑制再给氧时NO和脑细胞内[Ca2+]i的升高(P<0.05或P<0.01),16.0μmol·L-1的Hyp可将再给氧时NO和[Ca2+]i分别从(34.4±6.3)μmol·L-1和(640±94)nmol·L-1(Control组)降至(25.0±5.1)μmol·L-1(P<0.05)和(331±56)nmol·L-1(P<0.01)。结论Hyp对神经细胞缺氧/再给氧损伤保护作用可能与抑制NO的释放、钙超载及自由基脂质过氧化有关。     

The novel role and underlying mechanism of Wnt5a in regulating cellular cholesterol accumulation

Cholesterol accumulation is a critical step during the development and progression of atherosclerosis. Recently, Wnt5a expression has been found to be markedly upregulated in both murine and human atherosclerotic lesions. However, the effect and mechanism of Wnt5a in atherosclerosis is poorly understood. In the present study, we investigated the effects and potential mechanisms of Wnt5a on cholesterol accumulation during atherosclerosis. We used RAW264.7 and vascular smooth muscle cells (VSMC) treated with oxidized low‐density lipoprotein (oxLDL) as lipid‐loaded cell models. We found that expression of Wnt5a protein was increased in a concentration (25, 50, 75 and 100 μg/mL)‐ and time (24, 48 and 72 h)‐dependent manner by oxLDL treatment. To explore the underlying mechanism, we used Wnt5a short interference (si) RNA to knockdown Wnt5a expression in both RAW264.7 cells and VSMC, or applied recombinant Wnt5a (rWnt5a) to stimulate Wnt5a signalling. After Wnt5a knockdown, total cholesterol (TC) and free cholesterol (FC) content in both cell types increased significantly (P < 0.05) upon exposure to oxLDL. Conversely, the TC and FC content decreased markedly (P < 0.05) after treatment of cells with rWnt5a. More importantly, both protein and mRNA expression of Caveolin‐1 and ATP‐binding cassette transporter A1 (ABCA1) was significantly reduced after exposure of wnt5a siRNA‐treated cells to oxLDL, whereas rWnt5a treatment of cells resulted in increased Caveolin‐1 and ABCA1 protein expression after exposure of cells to oxLDL. Together, these findings demonstrate, for the first time, that Wnt5a reduces the accumulation of cholesterol in lipid‐loaded cells by regulating the mRNA expression of Caveolin‐1 and ABCA1, which are involved in reverse cholesterol transport. This may present a novel mechanism of Wnt5a‐mediated cholesterol transportation in macrophages and VSMC. Therefore, targeting the Wnt5a signalling pathway may have clinical implications in atherosclerosis.     

吡格列酮对人脐静脉内皮细胞CD40/CD40L表达的影响

目的探讨吡格列酮对氧化低密度脂蛋白(oxLDL)刺激下的人脐静脉内皮细胞(HUVECs)CD40/CD40L表达的影响。方法原代培养人脐静脉内皮细胞,给予oxLDL刺激和不同浓度吡格列酮干预。采用流式细胞技术检测CD40/CD40L在细胞上的表达,采用反转录-聚合酶链反应(RT-PCR)检测LOX-1mRNA的表达。结果OxLDL以浓度和时间依赖的方式刺激HUVECs表达CD40/CD40L,吡格列酮以剂量依赖的方式减轻ox-LDL刺激HUVECs表达CD40/CD40L。同时我们还观察到oxLDL能刺激HUVECs上调LOX-1mRNA的表达,而吡格列酮能明显抑制这种作用。结论吡格列酮能减轻oxLDL刺激下的人脐静脉内皮细胞CD40/CD40L的表达,其作用的机制可能与其抑制了HUVECs的LOX-1受体表达有关。     

Studies on the mechanism of SIRT1/AMPK signaling pathway between hepatocytes and hepatic stellate cells

OBJECTIVE To investigate the mechanism of SIRT1/AMPK signaling pathway between hepatocytes and hepatic stellate cells(HSCs).METHODS Normal human Chang liver cells and human hepatic stellate cell line,LX-2 cells were treated with SRT1720(10μmol·L~(-1))and AICAR(500μmol·L~(-1))prior to ethanol(50 mmol·L~(-1)) for 24 and 48 h.Cell viability was analyzed by methyl thiazolyl tetrazolium assay.SIRT1,AMPK and p-AMPK m RNA levels for 24 h and 48 h were analyzed by RT-PCR,SIRT1,AMPK and p-AMPK protein expressions in the supernatant at 24 and 48 h was detected by Western blot.RESULTS SRT1720 and AICAR effectively decreased LX-2 cell viabilities and exhibited scarcely little toxicity in human Chang liver cells.SRT1720 and AICAR attenuated collagen-I,α-smooth muscle actin(α-SMA)levels,activated liver kinase B-1(LKB1)and AMPK phosphorylation in ethanol treated LX-2 cells.Meanwhile,SRT1720 and AICAR enhanced SIRT1 expression mediated by ethanol both in Chang liver cells and LX-2 cells.Furthermore,SRT1720 and AICAR suppressed the expression of sterol regulatory element-binding protein-1(SREBP-1)to regulate fatty acid synthesis.CONCLUSION SIRT1 agonist and AMPK agonist blocked the crosstalk between hepatocytes and HSCs via SIRT1/AMPK signaling pathway to modulate hepatocytes accumulation of lipid and HSCs activation.     

Screening inhibitory effects of flavonoids isolated from Artemisia sacrorum on lipid accumulation in 3T3-L1 cells

OBJECTIVE To investigated the inhibitory effects of 12 flavonoids(compound 1-12: jaceosidin, kaempferol, chrysoeriol, quercetin, apigenin, hispidulin, luteolin,quercitrin, rutin, isorhamnetin, genkwanin, acacetin),which we had isolated from Artemisia sacrorum Ledeb.on lipid accumulation in 3T3-L1 cells. METHODS In screening experiments, the cells viability of these 12 flavonoids on the mouse preadipocyte 3T3-L1 cells were determined by MTS. The lipid accumulation and triglyceride(TG) levels were measured by Oil-Red O staining and TG test kit. RESULTS The MTS results showed that 1 and 4 have no toxicity on 0-10 μmol·L~(-1), 6 and 8 on 0-20 μmol·L~(-1), other compounds on 0-40 μmol·L~(-1). And OilRed O staining indicated that 1, 3, 5, 6, 7, 8, 10, 11 and12 inhibited the foramtion of lipid "ring" compared with model group. Further determined the content of TG manifested that compared with model group, the TG levels of1, 3, 5, 6, 7, 8, 10, 11 and 12 reduced to 51.6%, 60.6%,55.6%, 62.8%, 61.2%, 68.1%, 44.2%, 63.2% and 42.1%.CONCLUSION The compound of Jaceosidin, chrysoeriol,apigenin, hispidulin, luteolin, quercitrin isorhamnetin, genkwanin and acacetin have potential anti-adipogenic effects.     

Escin enhances anti-rheumatoid arthritis effects of low dose glucocorticoids through up-regulation of glucocorticoid receptor

OBJECTIVE To investigate the anti-rheumatoid arthritis(RA) effect of Escin combined with low dose of GCs(dexamethasone, Dex) and its underlying mechanism. METHODS Adjuvant-induced rheumatoid arthritis rats and LPS-injured RAW 264.7 were used to investigate the anti-RA effects of Escin combined with low dose Dex in vivo and in vitro. In vivo experiment: rats were randomly divided into model group(AIA), dexamethasone high dose(Dex, 0.2 mg·kg~(-1)) group, dexamethasone low dose(Dex, 0.05 mg·kg~(-1))group, Escin 10 mg·kg~(-1) group, Dex 0.05+Escin group, 10 rats in each group, another 10 were used as normal control group. The vehicle and the corresponding drug were administered intragastrically(ig) daily for 14 d. In vitro experiment: LPS was used to stimulate RAW264.7 macrophages for inflammatory models, which were divided into control group, LPS group, Dex with high dose(50 nmol·L~(-1))group, and Dex with low dose(12.5 nmol·L~(-1)) group. In the Escin 10 μmol·L~(-1) group and the Dex+Escin(12.5 nmol·L~(-1)+10 μmol·L~(-1))group, the corresponding drugs were added to each well. After 2 h, LPS was added to induce inflammation. RESULTS Escin combined with low dose Dex significantly decreased arthritic index, serum IL-6 and TNF-α, improved paw swelling, and ameliorated the joint pathology immune organ pathology significantly. Gene chip results revealed that Nr3 c1(GR) altered significantly. And that GR activation by Escin and low dose Dex was confirmed both in vivo and in vitro. Furthermore, Escin combined with low dose Dex also significant increase GR mRNA expression. However, when suppression of GR by its specific inhibitor, the anti-RA effect of Escin combined with low dose Dex was abolished. CONCLUSION Escin combined with Dex reduces the dose of Dex, and exerts significant anti-RA effects,which could also reduce the adverse effects of Dex. This combination might be attributed to GR activation. This study might provide a new combination drugs for the treatment of RA.