黄芪和三七的主要有效成分配伍对脑缺血/再灌注小鼠NF-κB信号通路及炎性因子表达的影响

目的从炎症反应探讨黄芪和三七主要有效成分配伍抗脑缺血/再灌注损伤的机制。方法将C57BL/6小鼠随机分为假手术组、模型组、黄芪甲苷(ASTⅣ)组、人参皂苷Rg1(Rg1)组、人参皂苷Rb1(Rb1)组、三七皂苷R1(R1)组、4种有效成分配伍组、ASTⅣ+Rg1组、ASTⅣ+Rb1组、ASTⅣ+R1组及阳性对照药依达拉奉组。预先给药3 d,末次给药1 h后,结扎双侧颈总动脉,造成脑缺血20 min,再灌注24h。RT-PCR法测定TNF-α、IL-1β、ICAM-1 mRNA表达,Western blot法测定脑组织p-IκBα蛋白及胞质、胞核NF-κB蛋白表达,计算NF-κB核转位率。结果 1脑缺血/再灌注后,脑组织TNF-α、IL-1β、ICAM-1 mRNA表达增加。ASTⅣ可降低TNF-αmRNA表达,Rg1可降低ICAM-1 mRNA的表达,R1能同时下调TNF-α、ICAM-1 mRNA的表达。ASTⅣ与Rg1、Rb1、R1配伍对TNF-α、IL-1β、ICAM-1 mRNA的表达均有不同程度的抑制作用,且以4种有效成分配伍组和ASTⅣ+R1组对炎性细胞因子表达的抑制效应更加明显。2脑缺血/再灌注后,脑组织p-IκBα蛋白表达明显增加,胞质NF-κB蛋白表达明显减少,而胞核NF-κB蛋白表达增加,NF-κB核转位率升高。ASTⅣ、Rg1、R1及各有效成分配伍均能抑制IκB磷酸化,减少NF-κB核转位的发生,且配伍组的效应大于各有效成分单用,4种有效成分配伍组的效应大于ASTⅣ+Rb1和ASTⅣ+Rg1组。结论黄芪和三七的主要有效成分配伍能通过抑制缺血/再灌注后脑组织NF-κB信号通路的激活,减少炎性细胞因子的生成,从而减轻脑缺血后脑组织的继发性炎症反应,发挥对脑组织的保护作用。     

丹参酮ⅡA对TNF-α诱导的ECV304细胞NF-κB、IκB-α表达及粘附分子ICAM-1、VCAM-1mRNA表达的影响

目的探讨丹参酮ⅡA对血管内皮细胞株ECV304NF-κB、IκB-α及粘附分子ICAM-1、VCAM-1mRNA表达的影响,以阐明其抗动脉粥样硬化作用及机制。方法通过建立TNF-α诱导的ECV-304细胞损伤模型,以抗氧化剂吡咯烷二硫代氨基甲酸盐(PDTC)做为对照,间接细胞ELISA方法定量检测NF-κB、IκB-α的表达,RT-PCR方法检测各组细胞ICAM-1、VCAM-1mRNA的表达。结果TNF-α可增加ECV304细胞转录因子NF-κB的表达,同时降低其抑制因子IκB-α的表达,低浓度的丹参酮ⅡA对TNF-α引起的ECV304细胞NF-κB的表达升高无明显抑制作用,但可增加其IκB-α的表达;高浓度的丹参酮ⅡA可明显抑制NF-κB的表达,同时增加其抑制因子IκB-α的表达。同时丹参酮ⅡA抑制TNF-α诱导的ECV304细胞ICAM-1、VCAM-1mRNA表达。结论丹参酮ⅡA可通过抑制转录因子NF-κB的激活及其相关粘附分子ICAM-1、VCAM-1mRNA表达,这有利于抑制动脉粥样硬化过程中的炎症从而发挥抗动脉粥样硬化作用。     

三七总皂苷对烫伤后核因子—κB及肿瘤坏死因子的影响

目的观察不同剂量的三七总皂苷对严重烫伤小鼠腹腔巨噬细胞内核因子-κB(NF-κB)活性及肿瘤坏死因子(TNF-α)mRNA的影响,阐明三七总皂苷对巨噬细胞分泌TNF-α影响的机制,探索体外运用该药的最佳剂量。方法以15%体表面积Ⅲ度烫伤小鼠为模型,收集腹腔巨噬细胞,电泳迁移率改变分析法测NF-κB的活性,反转录PCR测TNF-αmRNA的表达。结果烫伤后巨噬细胞内NF-κB活性与TNF-αmRNA的表达均显著升高,三七总皂苷在一定的浓度范围内呈剂量依赖性的抑制NF-κB活性与TNF-αmRNA的表达,以0.8mg*mL-1的剂量最明显,两者变化趋势相类似。结论三七总皂苷可能通过抑制NF-κB活性而降低TNF-αmRNA的表达。     

NF-κB p65 siRNA对延迟性排斥反应的抑制作用

目的 探讨核因子kappa B(NF-κB) p65的小干扰RNA (siRNA)对延迟性排斥反应的抑制作用.方法血管内皮细胞(EOMA)分为7组:A组(空白对照),B组(阴性对照),C组(TNF-α处理),D组(siRNA处理),E组(scramble siRNA处理),F组(TNF-α+ siRNA处理),G组(TNF-α+scramble siRNA处理).用阳离子脂质体LipofectamineTM 2000作为转染试剂将化学合成的小鼠NF-κB p65 siRNA转染入相应的EOMA细胞,24 h后在C组、F组和G组中加入TNF-α(终浓度为20 ng/ml).于TNF-α加入后的6h提取各组细胞总RNA,RT-PCR法测定EOMA细胞内E选择素(E-selectin)、细胞间黏附分子1(ICAM-1)、白细胞介素1α(IL-1α)和血管细胞黏附分子1(VCAM-1)水平.结果 F组EOMA细胞内E-selectin、ICAM-1、IL-1α和VCAM-1表达明显高于A组,的明显低于C组和G组(P＜0.01).结论 特异性siRNA抑制NF-κB p65表达可以有效抑制延迟性排斥反应.     

黄芪多糖通过抑制NF-κB和JNK信号通路减轻LPS诱导的小鼠心肌细胞凋亡

目的研究黄芪多糖(Astragalus polysaccharide,APS)对脂多糖(lipopolysaccharide,LPS)诱导的小鼠心肌细胞凋亡的影响,并探讨其作用机制。方法体外实验采用H9c2细胞预先给予APS,30 min后加入LPS(1 mg·L^-1)共孵育24 h,建立心肌细胞凋亡模型。体内实验采用SPF级昆明小鼠预防性给予APS 14 d后,腹腔注射LPS(10 mg·kg^-1)建立心肌细胞凋亡模型。8 h后采用超声心动测定小鼠心脏射血分数(EF)、左心室缩短分数(FS)等;TUNEL测心肌细胞凋亡;ELISA检测血清中IL^-1β、TNF-α含量;Western blot检测组织和体外心肌细胞中JNK、NF-κB信号通路及Bcl-2家族、caspase-3相关蛋白表达。结果 LPS能明显抑制小鼠的左心室收缩功能;促使心肌细胞凋亡;增加血清中IL^-1β、TNF-α,心肌细胞中JNK、p-JNK、Bax、caspase-3,胞核中NF-κB蛋白浓度;降低Bcl-2和胞质中NF-κB、IκB-α蛋白浓度。APS能明显保护LPS诱导的小鼠心肌收缩功能,减少心肌细胞凋亡;减少血清中IL^-1β、TNF-α,心肌组织细胞中p-JNK、Bax、caspase-3和胞核NF-κB蛋白含量;相对增加Bcl-2和胞质中NF-κB、IκB-α蛋白含量。而JNK蛋白表达无明显变化。结论 APS通过抑制NF-κB和JNK信号通路,减轻LPS诱导的小鼠心肌细胞凋亡。     

黄芩苷对脂多糖致内皮细胞炎症反应的保护作用及机制研究

目的研究黄芩苷对脂多糖(LPS)致人微血管内皮细胞(HMEC)炎症反应的保护作用及作用机制。方法采用LPS作用HMEC,建立炎症反应模型;以不同浓度的黄芩苷预处理细胞,然后将细胞暴露于LPS,ELISA检测炎症因子ICAM-1、IL-6和MCP-1的含量;荧光观察Ca^2+内流并采用流式细胞仪检测细胞内Ca^2+水平;免疫荧光法检测NF-κB p65入核情况;双荧光素酶报告基因方法检测NF-κB核内转录活性;Western blot检测NF-κB p65、p-NF-κB p65及TLR4的表达。结果HMEC暴露于LPS后,出现了明显的Ca^2+内流,NF-κB p65发生磷酸化,核内转录活性上调,ICAM-1、IL-6及MCP-1表达上调。不同浓度的黄芩苷均能抑制LPS刺激HMEC后产生的Ca^2+内流、NF-κB p65入核及核内转录活性上调,减少ICAM-1、IL-6、MCP-1的表达,下调NF-κB p65、p-NF-κB p65及TLR4的表达,且抑制作用呈现一定的量效关系。结论黄芩苷能抑制LPS诱导的HMEC炎症反应,其机制与抑制Ca^2+内流和NF-κB信号通路的活化,从而降低炎症反应的水平有关。     

银杏内酯B对脂多糖刺激的小鼠腹腔巨噬细胞TNFα生成及大鼠胸腔多形核白细胞NF-кB活化的影响

目的研究银杏内酯B对脂多糖刺激的小鼠腹腔巨噬细胞TNFα生成及大鼠胸腔多形核白细胞NF-κB活化的影响.方法用L929细胞结晶紫染色法检测TNFα的含量,用电泳迁移率改变检测法检测NF-κB的结合活性.结果1和10 μmol·L-1银杏内酯R能够显著抑制LPS刺激的小鼠腹腔巨噬细胞TNFα的生成,其IC50为0.26μmol·L-1:1 mg·L-1LPS和1 nmol·L-1PAF均可活化大鼠胸腔多形核白细胞NF-κB;银杏内酯B能够抑制LPS或PAF刺激的NF-κR活化.结论银杏内酯B能够抑制LPS刺激的小鼠腹腔巨噬细胞TNFα生成及大鼠胸腔多形核白细胞NF-κB的活化.PAF参与LPS激活NF-κB的过程.     

竹节参齐墩果烷皂苷对RAW264.7巨噬细胞SIRT1活性影响及抗炎作用研究

目的探讨竹节参齐墩果烷皂苷(chikusetsu oleanane saponin,COS)对脂多糖(lipopolysaccharides,LPS)刺激RAW264.7巨噬细胞的SIRT1活性影响及抗炎作用。方法Griess法测定一氧化氮(NO)释放量;免疫印迹(Western blot)法检测炎性因子肿瘤坏死因子-α(TNF-α)、白介素1β(IL-1β)蛋白表达;免疫荧光分析COS对细胞核因子-κB(NF-κB)和沉默信息调节因子1(silent information regulator1,SIRT1)核转运的作用。结果 COS在25~300 mg·L~(-1)与1 mg·L~(-1)LPS共培养时,对RAW264.7细胞生长无明显影响;与LPS组相比,COS能有效抑制NO释放和抑制TNF-α、IL-1β的分泌;还能抑制NF-κB的核移位,上调SIRT1的表达。结论 COS对LPS刺激的RAW264.7细胞炎症具有保护作用,其保护机制可能是COS上调SIRT1表达,促进NF-κB去乙酰化作用,从而抑制NF-κB的核移位,减少TNF-α、IL-1β等炎症因子的产生。     

Sanggenon C对人多形核白细胞和滑膜细胞粘附的抑制作用及其机制

目的:观察化合物Sanggenon C对人外周血多形核白细胞(PMN)与人滑膜细胞(HSC)粘附的抑制作用,并探讨其作用机制.方法:MTT比色法研究PMN与HSC粘附,Cell-ELISA及RT-PCR法研究HSC粘附分子ICAM-1和VCAM-1表达,EMSA研究核转录因子NF-κB的活化.结果:Sanggenon C在0.01-10μmol·L~(-1)范围内均可显著抑制TNF-α 5O kU·L~(-1)与IL-1β诱导的HSC与PMN粘附,其IC_(50)分别为27.29nmol. L~(-1)和54.45nmol·L~(-1);Sanggenon C可显著抑制HSC表面ICAM-1和VCAM-1蛋白表达,同时也显著抑制VCAM-1 mRNA表达,但对ICAM-1 mRNA表达无显著影响;Sanggenon C在1-10μmol·L~(-1)浓度下也可显著抑制TNF-α对NF-κB的活化.结论:Sanggenon C是一个有效的人PMN与HSC粘附抑制剂,其作用机制可能是通过抑制NF-κB的活化,进而抑制HSC表面VCAM-1的表达或抑制ICAM-1转录后调控过程而实现的.     

MYR通过NF-κκB信号通路改善LPS诱导小鼠纹状体炎症反应

目的研究MYR对LPS诱导小鼠纹状体内神经炎症的作用及机制。方法雄性BALB/c小鼠随机分为正常对照组、LPS模型组、MYR 20和50 mg·kg~(-1)给药组。连续给予MYR 7 d,于末次给药后,模型组和给药组小鼠采用腹腔注射LPS5 mg·kg~(-1)诱导小鼠急性神经炎症的发生,LPS注射6 h后,ELISA法检测小鼠纹状体中IL-1β,IL-6,TNF-α,MCP-1以及ICAM-1等炎症因子的变化;Western印迹法检测小鼠纹状体中NF-κB信号通路相关蛋白的表达变化。结果与正常对照组比较,LPS诱导组小鼠纹状体中炎症因子IL-1β,IL-6,TNF-α,MCP-1以及ICAM-1显著增加(所有P<0.01),NF-κB信号通路相关蛋白表达显著增加。而给予MYR 20和50 mg·kg~(-1)可显著抑制LPS诱导的小鼠纹状体炎症因子的释放,抑制NF-κB,IκB蛋白的磷酸化,抑制胞浆内NF-κB的核转位。结论 MYR可有效抑制LPS诱导的神经炎症,保护小鼠纹状体中多巴胺神经元,其抗炎保护作用与抑制NF-κB信号通路密切相关。     

Rhynchophylline prevents cardiac dysfunction and improves survival in lipopolysaccharide-challenged mice via suppressing macrophage I-κBα phosphorylation

Myocardial dysfunction is a common complication during sepsis and significantly contributes to the mortality of patients with septic shock. However, none of the available therapeutic strategies proven to be effective in patients with severe sepsis are designed specifically to target myocardial dysfunction. The purpose of the present study is to investigate the effect of rhynchophylline (Rhy) on LPS-induced myocardial dysfunction in mice. We found that pretreatment with Rhy significantly improved cardiac systolic dysfunction, increased stroke volume and cardiac output in mice challenged with LPS. LPS induced cardiac inhibitor-κBα (I-κBα) phosphorylation, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) mRNA expression, and in turn increased cardiac TNF-α and IL-1β protein production, all of which were attenuated by pretreatment with Rhy. Immunohistochemistry revealed that TNF-α was found in infiltrated macrophages (F4/80(+)) and myocardium, and Rhy reduced TNF-α immunostaining in cardiac infiltrated macrophages in LPS-challenged mice. Furthermore, Rhy inhibited LPS-induced I-κBα phosphorylation and TNF-α production in cultured mouse peritoneal macrophages, but not in neonatal mouse cardiomyocytes. Pretreatment with Rhy significantly decreased the mortality of LPS-challenged mice. These results indicate that Rhy reduces cardiac dysfunction and improves survival via suppression of macrophage I-κBα phosphorylation in LPS-challenged mice, and suggest that Rhy may be a potential agent for the treatment of septic cardiac dysfunction.     

腺苷对肿瘤坏死因子-α诱导乳鼠心肌细胞肥大及核因子-κB的影响

目的探讨腺苷对肿瘤坏死因子-α(tumor necrosis fac-tor,TNF-α)诱导心肌细胞肥大及核因子-κB(NF-κB)表达的影响。方法以原代培养乳鼠心肌细胞为模型,应用TNF-α100μg.L-1诱导心肌细胞肥大,观察不同浓度腺苷对心肌肥大的影响。用考马斯亮蓝法测定心肌细胞蛋白含量;RT-PCR检测心肌细胞心钠素(atrial natriuretic peptide,ANP)mRNA的表达;Western blot法检测心肌细胞p65和IκBα的蛋白含量;ELISA法检测细胞外液白介素-1β(IL-1β)的含量。结果腺苷能够有效抑制TNF-α诱导的心肌肥大,表现为蛋白含量减少,ANPmRNA表达降低,并且能抑制TNF-α诱导的NF-κB活化,表现为细胞内p65蛋白表达减少,IκBα蛋白表达增加和细胞外液IL-1β表达降低。结论腺苷对TNF-α诱导的心肌肥大有保护作用,可能与腺苷抑制心肌细胞NF-κB活化有关。     

DATS通过NF-κB抑制LPS诱导小鼠肺泡巨噬细胞促炎细胞因子表达

目的探讨二烯丙基三硫(DATS)抑制脂多糖(LPS)诱导小鼠肺泡巨噬细胞肿瘤坏死因子-α(TNF-α)及白介素-1β表达的信号转导机制。方法体外培养MH-S细胞,用DATS和(或)LPS进行干预。反转录PCR检测细胞中TNF-α、IL-1β mRNA表达,电泳迁移率改变分析(EMSA)检测细胞核因子-κB(NF-κB)活性,Western blot检测细胞磷酸化(p-IκB)及非磷酸化IκB的表达。结果LPS刺激MH-S细胞可导致TNF-α、IL-1β mRNA、p-IκB表达增加及NF-κB活性升高。用DATS(0.1、0.5、2.5、5.0mg.L-1)预处理细胞30min后再给予LPS刺激,可使TNF-α、IL-1β mRNA表达降低,并呈剂量依赖性;升高的NF-κB活性及p-IκB表达均显不同程度的抑制。单独DATS对TNF-α、IL-1β mRNA表达及NF-κB活性无影响。结论DATS可通过抑制IκB磷酸化及NF-κB活化,进而下调LPS诱导小鼠肺泡巨噬细胞TNF-α、IL-1β mRNA表达。     

Schisandrin B inhibits LPS-induced inflammatory response in human umbilical vein endothelial cells by activating Nrf2

Schisandrin B (SchB), an active ingredient extracted from Schisandra chinensis (Turcz.) Baill, has been known to have anti-oxidant and anti-inflammatory activities. In this study, we investigated the anti-inflammatory effects and mechanism of SchB in LPS-stimulated human umbilical vein endothelial cells (HUVECs). The effects of SchB on VCAM-1, ICAM-1, NF-κB and Nrf2 expression were detected by western blot analysis. The effects of SchB on TNF-α and IL-8 production were detected by ELISA. The results showed that SchB strongly suppressed the production of TNF-α and IL-8 in HUVECs stimulated with LPS. SchB also inhibited LPS-induced VCAM-1 and ICAM-1 expression. Furthermore, SchB blocked the activation of NF-κB induced by LPS. In addition, SchB increased the expression of Nrf2 and HO-1 in a concentration-dependent manner. And the inhibition of TNF-α and IL-8 production by SchB was blocked by transfection with Nrf2 siRNA. Our findings showed that SchB inhibited LPS-induced inflammation in HUVECs by activating Nrf2 signaling pathway.     

DATS通过p38MAPK通路抑制LPS诱导的小鼠MH-S细胞TNF-α及IL-1β表达

目的探讨p38MAPK在二烯丙基三硫(DATS)抑制脂多糖(LPS)诱导小鼠肺泡巨噬细胞促炎细胞因子表达中的作用。方法体外培养MH-S细胞,用DATS和(或)LPS进行干预,Western blot检测细胞p38及磷酸化p38(p-p38)的表达;用LPS和(或)SB203580孵育细胞,反转录PCR检测细胞中TNF-α、IL-1βmRNA表达,Western blot检测细胞磷酸化(p-IκB)及非磷酸化IκB的表达。结果 LPS刺激MH-S细胞可导致p-p38表达增加,呈时间依赖性;用DATS(0.1、0.5、2.5、5.0 mg.L-1)预处理细胞30 min后再给予LPS刺激,p-p38表达呈剂量依赖性下降;单独DATS对p-p38表达无明显影响。p38特异性抑制剂SB203580可剂量依赖性地抑制LPS诱导的p-IκB蛋白、TNF-α及IL-1βmR-NA表达。结论 DATS可通过抑制p38MAPK通路抑制IκB磷酸化及NF-κB活化,进而下调LPS诱导小鼠肺泡巨噬细胞TNF-α、IL-1βmRNA表达。     

Acanthoic acid inhibits LPS-induced inflammatory response by activating LXRα in human umbilical vein endothelial cells

Acanthoic acid, a pimaradiene diterpene isolated from Acanthopanax koreanum, has been reported to have anti-inflammatory activities. However, the effect of acanthoic acid on vascular inflammation has not been investigated. The aim of this study was to investigate the anti-inflammatory effects of acanthoic acid on lipopolysaccharide (LPS)-induced inflammatory response in human umbilical vein endothelial cells (HUVECs). The production of cytokines TNF-α and IL-8 was detected by ELISA. The expression of VCAM-1, ICAM-1, E-selectin, NF-κB and LXRα were detected by Western blotting. Adhesion of monocytes to HUVECs was detected by monocytic cell adhesion assay. The results showed that acanthoic acid dose-dependently inhibited LPS-induced TNF-α and IL-8 production. Acanthoic acid also inhibited TNF-α-induced IL-8 and IL-6 production. LPS-induced endothelial cell adhesion molecules, VCAM-1 and ICAM-1 were also inhibited by acanthoic acid. Acanthoic acid inhibited LPS-induced NF-κB activation. Furthermore, acanthoic acid dose-dependently up-regulated the expression of LXRα. In addition, our results showed that the anti-inflammatory effect of acanthoic acid was attenuated by transfection with LXRα siRNA. In conclusion, the anti-inflammatory effect of acanthoic acid is due to its ability to activate LXRα. Acanthoic acid may be a therapeutic agent for inflammatory cardiovascular disease.     

Withaferin A inhibits tumor necrosis factor-α-induced expression of cell adhesion molecules by inactivation of Akt and NF-κB in human pulmonary epithelial cells

We here investigated the functional effect of withaferin A on airway inflammation and its action mechanism. Withaferin A inhibited the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in human lung epithelial A549 cells stimulated with tumor necrosis factor-α (TNF-α), resulting in the suppression of leukocyte adhesion to lung epithelial A549 cells. In addition, withaferin A inhibited TNF-α-induced expression of adhesion molecules (ICAM-1 and VCAM-1) protein and mRNA in a dose-dependent manner. Withaferin A prevented DNA binding activity of nuclear factor-κB (NF-κB) and nuclear translocation of NF-κB. It also inhibited phosphorylation of Akt and extracellular signal-regulated kinase (ERK), which are upstream in the regulation of adhesion molecules by TNF-α. Furthermore, withaferin A inhibited U937 monocyte adhesion to A549 cells stimulated by TNF-α, suggesting that it may inhibit the binding of these cells by regulating the expression of critical adhesion molecules by TNF-α. Taken together, these results suggest that withaferin A inhibits cell adhesion through inhibition of ICAM-1 and VCAM-1 expression, at least in part, by blocking Akt and down-regulating NF-κB activity.     

熵权法结合星点设计-效应面法优化祛湿清肺方提取工艺及体外抗炎活性评价

目的:优化祛湿清肺方提取工艺,并对祛湿清肺方提取液进行体外抗炎活性评价。方法:以绿原酸、虎杖苷、黄芩苷、汉黄芩苷、黄芩素、芦荟大黄素、汉黄芩素、大黄素成分含量及得膏率为指标,加水量及提取时间为考察因素,采用熵权法结合星点设计-效应面法对祛湿清肺方提取工艺进行优化。以脂多糖(LPS)诱导大鼠腹腔巨噬细胞(RAW_264.7)为炎症模型,酶联免疫吸附法测定白细胞介素-6(interleukin-6,IL-6)、白细胞介素-1β(interleukin-1β,IL-1β)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、一氧化氮(NO)的含量,蛋白质印迹法检测磷酸化NF-κB抑制蛋白激酶(phosphorylated inhibitor of NF-κB kinase,p-IKK)、磷酸化NF-κB p65(phosphorylated NF-κB p65,p-NF-κB p65)、NF-κB抑制蛋白α(inhibitor of NF-κBα,IκBα)蛋白表达水平变化,评价祛湿清肺方提取液抗炎活性。结果:星点设计-效应面法优化所得的最佳提取工艺为加水量13倍,提取2次,每次提取时间105 min。祛湿清肺方提取液能降低IL-6、IL-1β、TNF-α、NO的含量,抑制p-IKK、p-NF-κB p65蛋白表达,促进IκBα蛋白表达,具有较好的体外抗炎活性。结论:熵权法结合星点设计-效应面法优选的祛湿清肺方提取工艺稳定可行,所得提取液具有较好的抗炎活性,为祛湿清肺方开发和现代化研究提供参考奠定基础。     

姜黄素通过阻断NF-κB减少IL-1β诱导的内皮脂酶表达

目的观察姜黄素对培养的人血管内皮细胞内皮脂酶表达的影响,并探讨其可能的作用机制。方法不同浓度的姜黄素处理HUVEC-12细胞。RT-PCR检测内皮酯酶(endo-thelial lipase,EL)mRNA的表达;Western blot检测核因子-κB抑制因子-α(inhibitor of nuclear factor-κB-α,IκB-α)蛋白的表达;间接免疫荧光检测核因子-κB(nuclear factor-κB,NF-κB)蛋白的活化。结果IL-1β处理HUVEC-12细胞可以明显上调EL mRNA的表达,同时降低胞质蛋白IκB-α的表达水平,激活核转录因子NF-κB,增加胞核蛋白NF-κB的水平。姜黄素预处理HUVEC-12细胞可以抑制IL-1β对EL的上调作用,同时逆转IL-1β诱导的IκB-α蛋白降解和NF-κB活化。结论姜黄素可以通过阻断NF-κB活化减少IL-1β诱导的人血管内皮细胞EL的表达。