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Chinese Journal of Integrative Medicine 2019年第9期25卷 663-670页

作者： ZHOU Qi YU Dong-hua ZHANG Ning LIU Shu-min Research Institute of Chinese Medicine Heilongjiang University of Chinese Medicine Harbin 150040 China Technological Innovation Team of Basic Theory Study Research of Institution of Higher Education in Heilongjiang Province Heilongjiang University of Chinese Medicine Harbin 150040 China

Objective: To investigate the mechanism of Chinese herbal medicine Dioscorea nipponica for the treatment of monosodium urate crystals-induced gouty arthritis(GA) in rats. Methods: Sixty male Wistar rats were divided into 6 groups: normal, model, indomethacin and three total saponin(900, 300 and 100 mg/kg) groups. The liver, kidney and serum levels of lysosomal enzymes, antioxidant capacities, and inflammatory factors were measured. In addition, the m RNA and protein levels of the nalp3 inflammasome components in the mononuclear cells of rats’ peripheral blood were analyzed using real-time polymerase chain reaction and Western blotting methods, respectively. Results: Total saponins groups could reduce the activities of β-galactosidase,β-N acetyl glucosamine enzyme,β-glucuronidase, acid phosphatase, and malonaldehyde as wel as the contents of TNF-α, IL-1β and IL-8(all Pnalp3 in the mononuclear cells of peripheral blood(all Pnalp3 inflammasome.

关键词： apoptosis-associated speck-like protein containing a caspase-recruitment domain caspase-1 Chinese medicine Dioscorea nipponica nalp3

Expression of nalp3 in the Spleen of Mice with Portal Hypertension

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2010年第2期30卷 170-172页

作者：夏泽锋王国斌万赤丹刘涛王帅王博程锐 Department of General Surgery Union HospitalTongji Medical CollegeHuazhong University of Science and Technology

This study examined the mRNA expression of nalp3 in the spleen of the mice with hypersplenism due to portal hypertension （PH）. The mouse hypersplenism models were established by oral administration of tetrachloromethane （2 mL/kg/week for 12 weeks by oral gavage）. All the mice were randomly divided into a control group and an experimental group. The blood routine test was conducted, spleen index was calculated and spleen was histologically examined. Portal vein sera were taken for detection of the level of uric acid. The mRNA expressions of nalp3 and IL-1β in the spleen were detected by reverse transcriptase-polymerase chain reaction （RT-PCR）. The results showed that the platelet count was significantly lower in the experimental group [（674±102）× 10^9/L] than in the control group [（1307±181） × 10^9/L] （P〈0.05）, while the spleen index was significantly higher [（9.83 ±1.36） μg/g] in the experimental group than in the control group [（4.11 ±0.47） μg/g] （P〈0.05）. The histopathological changes of spleen followed the pattern of congestive splenomegaly. No significant difference was found in the uric acid level in the portal vein between the control group and the experiment group. The mRNA expressions of nalp3 and IL-1β were up-regulated significantly in the spleen in the experimental group as compared with those in the control group （P〈0.05）. It was concluded that nalp3 and IL-1β may play important roles in the pathogenesis of hypersplenism.

关键词： nalp3 interleukin-1β hypersplenism hypertension, portal

Histone deacetylase 6 mediated nalp3 inflammasome activation contributes to dopaminergic injury in experimental models of Parkinson disease

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中国药理学与毒理学杂志 2018年第9期32卷 686-687页

作者： YAN Shao-qi WEI Xin-bing JIAN Wen-cheng QIN Yue JIANG Fan LOU Hai-yan ZHANG Bin Department of Pharmacology School of Basic Medical SciencesShandong University Jinan 250012China Department of Radiology Qilu HospitalShandong University Jinan 250012China Department of Pathophysiology School of Basic Medical SciencesShandong University Jinan 250012China

OBJECTIVE To investigate the mechanisms of histone deacetylase 6(HDAC6)deacetylation activity on nalp3 inflammasome activation and explore the protective effect s of pharmacological inhibition of HDAC6 on dopaminergic *** In vitro and in vivo6-OHDA induced Parkinson disease(PD) model was *** distinguish the effect of deacetylase catalytic domains of HDAC6,we used a specific HDAC6 inhibitor tubastatin A(TBA),siRNAHDAC6,and pcDNA-HDAC6-FLAG ***,the role of pharmacological inhibition or siRNA or overexpression of HDAC6 on nalp3 inflammasome and cell death was explored by using Western blotting,TUNEL,and flow cytometric ***,the acetylation level of peroxiredoxin 2(Prx2) and the production of reactive oxygen species(ROS) in cells under different treatments was examined by using immunoprecipitation and DCFH-DA fluorescence *** effects of TBA on neuroinflammation and nigrostriatal dopaminergic system in vivo was further investigated by using Western blotting,immunohistochemistry and HPLC *** TBA remarkably inhibited 6-OHDA induced nalp3 inflammasome activation,reduced dopaminergic neurodegeneration and neuroinflammation as demonstrated by increased TH-positive neurons,striatal levels of DA and its metabolites,and decreased gliocyte *** recovered acetylation of Prx2,and reduced ROS production,which was associated with decreased nalp3 inflammasome *** HDAC6 may medicate deacetylation of Prx2 contributes to nalp3 inflammasome activation in PD pathology,suggesting that the development of specific pharmacological inhibitors of HDAC6 be required for this kind of disease.

关键词： histone deacetylase 6 nalp3 peroxiredoxin 2 reactive oxygen species

Inflammasome-independent nalp3 contributes to high-salt induced endothelial dysfunction

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中国药理学与毒理学杂志 2019年第10期 796-797页

作者： FU Hui CHEN Ji-kuai LU Wen-jie JIANG Yu-jie WANG Yuan-yuan LI Dong-jie SHEN Fu-ming Department of Pharmacy Shanghai Tenth People′ s Hospital Tongji University Department of Health Toxicology Faculty of Naval Medicine Second Military Medical University

OBJECTIVE Na+is an important nutrient and its intake, mainly from salt（Na Cl）, is essential for normal physiological function. However, high salt intake may lead to vascular injury, independent of a rise in blood pressure（BP）. Canonical nalp3 inflammasome activation is a caspase-1 medicated process, resulting in the secretion of IL-18 and IL-1β which lead to endothelial dysfunction. However, some researches uncovered a direct and inflammasome-independent role of nalp3 in renal injury. Thus, this study was designed to investigate the possible mechanisms of nalp3 in high salt induced endothelial dysfunction. METHODS and RESULTS Changes in endothelial function were measured by investigating mice(C57 BL/6 J, nalp3;and wild-type, WT)fed with normal salt diet（NSD） or high-salt diet（HSD） for12 weeks, and thoracic aortic rings from C57 BL/6 J mice cultured in high-salt medium. Changes of tube formation ability, intracellular reactive oxygen species（ROS）, and nalp3 inflammasome expression were detected using mouse aortic endothelial cells（MAECs） cultured in highsalt medium. Consumption of HSD for 12 weeks did not affect BP or body weight in C57 BL/6 J mice. Endotheliumdependent relaxation（EDR） decreased significantly in C57 BL/6 J mice fed with HSD for 12 weeks, and in isolated thoracic aortic rings cultured in high-salt medium for 24 *** from the aortic ring assay also revealed that the angiogenic function of thoracic aortas was impaired by either consumption of HSD or exposure to high-salt medium. nalp3;mice fed with HSD showed a relatively mild decrease in EDR function when compared with WT mice. Tube length of thoracic aortic rings from nalp3;mice was longer than those from WT mice after receiving high-salt treatment. Inhibiting nalp3 with a nalp3 antagonist, smal interfering（si） RNA experiments using si-Rnalp3,and decomposing ROS significantly improved tube formation ability in MAECs under high salt medium. nalp3 expression was increased in MAECs cultured with hig

关键词： high salt intake endothelial-dependent relaxation angiogenic function nalp3 reactive oxygen species

nalp3炎性复合体及ERK信号通路在氧化应激中的作用及阿魏酸钠的干预机制

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四川大学学报（医学版） 2016年第5期47卷 655-659,690页

作者：魏小林谢敏何高燕四川大学华西医院呼吸内科成都610041

目的探讨氧化应激时人肺上皮细胞(A549)中nalp3炎性复合体、细胞外调节蛋白激酶(ERK)的表达变化,阿魏酸钠(SF)的干预作用及其可能的机制。方法培养A549细胞,分为空白对照组,H2O2刺激组,阿魏酸钠组,caspase-1抑制剂(Z-VAD)组,ERK阻断剂(P... 详细信息

目的探讨氧化应激时人肺上皮细胞(A549)中nalp3炎性复合体、细胞外调节蛋白激酶(ERK)的表达变化,阿魏酸钠(SF)的干预作用及其可能的机制。方法培养A549细胞,分为空白对照组,H2O2刺激组,阿魏酸钠组,caspase-1抑制剂(Z-VAD)组,ERK阻断剂(PD98059)组,阿魏酸钠+H2O2组。其中H2O2刺激组用H2O2 200μmol/L培养细胞2h,阿魏酸钠组用阿魏酸钠400μg/mL处理细胞30 min,Z-VAD组、PD98059组、阿魏酸钠+H2O2组分别用Z-VAD 20μmol/L、PD98059 50μmol/L、阿魏酸钠400μg/mL预处理A549细胞30min后加入H2O2200μmol/L培养2h,采用实时荧光定量PCR检测各组A549中caspase-1、nalp3mRNA的表达,Western blot检测caspase-1、nalp3、磷酸化ERK(p-ERK)、ERK蛋白含量;ELISA法检测各组A549上清液中白细胞介素-1β(IL-1β)含量。结果与空白对照组比较,H2O2可使A549细胞caspase-1、nalp3mRNA及caspase-1、nalp3、p-ERK/ERK蛋白水平表达增强,IL-1β分泌增加(P均0.05)。与H2O2刺激组比较,Z-VAD组、PD98059组和阿魏酸钠+H2O2组caspase-1、nalp3mRNA及蛋白表达降低,p-ERK/ERK蛋白表达降低,IL-1β分泌下降(P均0.05)。结论阿魏酸钠可能通过抑制ERK活化,减少caspase-1、nalp3及IL-1β的表达,从而减轻氧化应激导致的炎症级联反应。

关键词： H2O2 人肺上皮细胞A549 nalp3 Caspase-1 ERK 阿魏酸钠

nalp3及NF-κB信号通路在氧化应激反应中的作用及阿魏酸钠的干预效应

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四川大学学报：医学版 2015年第3期46卷 367-371页

作者：何高燕谢敏高艳黄建戈四川大学华西医院呼吸内科成都610041

目的检测氧化应激时人肺上皮细胞(A549)炎性复合体nalp3、核转录因子-kappa B(NF-κB)基因和蛋白的表达,探讨阿魏酸钠对其的干预作用及可能的作用机制。方法培养A549细胞,分为对照组、H2O2(100μmol/L)应激组、NF-κB阻断剂组(PDTC+H2O2... 详细信息

目的检测氧化应激时人肺上皮细胞(A549)炎性复合体nalp3、核转录因子-kappa B(NF-κB)基因和蛋白的表达,探讨阿魏酸钠对其的干预作用及可能的作用机制。方法培养A549细胞,分为对照组、H2O2(100μmol/L)应激组、NF-κB阻断剂组(PDTC+H2O2组)、阿魏酸钠干预组(阿魏酸钠+H2O2组),其中PDTC(100μmol/L)和阿魏酸钠(400μg/mL)预处理30min后加入H2O2(100μmol/L),培养2h后,采用实时荧光定量-PCR(qRT-PCR)检测nalp3、NF-κB(P65)mRNA的表达;Western blot检测nalp3、IκBα蛋白的表达;酶联免疫吸附(ELISA)测定细胞上清中白介素-1β(IL-1β)的表达。结果与对照组比较,H2O2可使A549细胞nalp3mRNA、nalp3蛋白水平表达增强,NF-κB(P65)mRNA表达上调、IκBα降解增强,IL-1β分泌增加(P均nalp3mRNA、nalp3蛋白、NF-κB(P65)mRNA表达,IκBα降解减少,IL-1β分泌下降(P均nalp3及IL-1β的表达,从而减轻氧化应激导致的炎症反应。

关键词： H2O2 人肺上皮细胞A549 nalp3 NF-κB IL-1β 阿魏酸钠

游离脂肪酸对THP-1巨噬细胞nalp3炎性通路的影响

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中南大学学报（医学版） 2014年第8期39卷 811-817页

作者：付丽瑶周伏喜王学红卢放根中南大学湘雅二医院消化内科长沙410011

目的:探讨nalp3炎性小体在非酒精性脂肪性肝炎(non-alcoholic steatohepatitis,NASH)的炎症发生发展中的可能作用。方法:选择THP-1构建体外巨噬细胞模型,用不同浓度的棕榈酸干预24 h;用不同浓度的N-乙酰半胱氨酸(N-acetylcysteine,NAC)... 详细信息

目的:探讨nalp3炎性小体在非酒精性脂肪性肝炎(non-alcoholic steatohepatitis,NASH)的炎症发生发展中的可能作用。方法:选择THP-1构建体外巨噬细胞模型,用不同浓度的棕榈酸干预24 h;用不同浓度的N-乙酰半胱氨酸(N-acetylcysteine,NAC)预处理细胞后加入高浓度的棕榈酸孵育24 h。分别用活性氧(reactive oxygen species,ROS)指示剂结合流式细胞仪检测THP-1中ROS的变化;ELISA检测细胞上清液中IL-1β的浓度;免疫荧光技术检测nalp3,caspase-1蛋白的表达;荧光定量PCR检测nalp3蛋白复合体各组分(nalp3,ASC,caspase-1)mRNA的表达水平。结果:与空白组相比,各棕榈酸组细胞内ROS增加,nalp3和caspase-1蛋白表达及其分泌IL-1β水平均增加(Pnalp3和caspase-1蛋白表达水平,nalp3复合体各组分mRNA水平及其分泌IL-1β的能力均降低(Pnalp3炎性小体信号通路的活化引起炎症因子分泌,该通路可能是NASH的发病机制之一。

关键词：棕榈酸 THP-1巨噬细胞活性氧 nalp3 炎性小体

nalp3-siRNA对缺氧复氧诱导大鼠肾小管上皮细胞损伤的保护作用及其机制

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中华肾脏病杂志 2012年第11期28卷 873-878页

作者：冯娟李荣山乔晞郝洁芦王卫赵宏宇邵珊山西医科大学第二临床医院肾内科太原030000

目的通过构建nalp3-siRNA，观察其抑制大鼠。肾小管上皮细胞（NRK-52E）nalp3表达的作用，探讨其对细胞缺氧复氧（HR）损伤的保护作用。方法（1）利用三气培养箱调整氮气压力条件形成缺氧条件，缺氧1h，按复氧时间设复氧后1、2、4、8、1... 详细信息

目的通过构建nalp3-siRNA，观察其抑制大鼠。肾小管上皮细胞（NRK-52E）nalp3表达的作用，探讨其对细胞缺氧复氧（HR）损伤的保护作用。方法（1）利用三气培养箱调整氮气压力条件形成缺氧条件，缺氧1h，按复氧时间设复氧后1、2、4、8、16、24h组，分别检测细胞培养上清液中的乳酸脱氢酶（LDH）含量以及细胞nalp3蛋白的表达。（2）NRK-52E转染nalp3-siRNA质粒，Western印迹法检测转染细胞nalp3蛋白的表达。（3）将细胞分为正常对照组、HR组、无关siRNA转染组和nalp3-siRNA转染组。分别于缺氧1h、复氧4h检测培养液上清LDH的含量和细胞nalp3蛋白的表达。（4）采用Annexin V／PI染色结合流式细胞仪、Western印迹法、电泳迁移率实验（EMSA）分别检测细胞凋亡率、细胞IκB-α、Bax和Bel-2蛋白的表达以及NF-κBDNA结合活性。结果（1）与对照组相比，NRK-52E缺氧复氧后活细胞计数和细胞存活率显著下降（P〈0．05），细胞nalp3表达增加，在复氧4h达到高峰。（2）与无关siRNA转染组相比，nalp3-siRNA转染组nalp3蛋白表达水平显著下调（P〈0．05）。（3）缺氧复氧后，与无关siRNA转染组相比，NRK-52E细胞nalp3蛋白表达显著下降（P〈0．05）。（4）与对照组比较，HR后细胞IκB-d磷酸化和降解以及NF-κBDNA结合活性增加，细胞nalp3、Bcl-2和Bax蛋白的表达明显上调，而nalp3-siRNA转染组细胞IκB-α蛋白的降解，NF-κBDNA结合活性以及Bax／Bcl-2蛋白的比值均低于无关siRNA转染组（均P〈0．05）。同时，各组细胞凋亡率也明显增多，其中nalp3-siRNA转染组细胞凋亡率明显低于无关siRNA转染组（均P〈0．05）。结论nalp3-siRNA能够显著抑制肾小管上皮细胞内nalp3的表达，对肾小管上皮细胞缺氧复氧损伤有一定的保护作用。其机制可能通过抑制nalp3表达，对NF-κB的活化以及Bcl-2和Bax蛋白表达的不同调控，减少细胞的凋亡。

关键词：再灌注损伤细胞凋亡肾小管上皮细胞 nalp3 NF-κB Bcl-2

萆薢总皂苷对大鼠急性痛风性关节炎nalp3炎性体信号通路的影响

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中国药理学通报 2017年第3期33卷 354-360页

作者：王璐那莎陈光亮安徽中医药大学中西医结合临床学院安徽合肥230038

目的研究萆薢总皂苷对大鼠急性痛风性关节炎的防治作用及机制。方法 Wistar大鼠,♂,72只,随机分组后,各用药组大鼠预先灌胃给予不同剂量萆薢总皂苷,随后右侧踝关节腔注射尿酸钠诱导急性痛风性关节炎。观察大鼠步态,测定关节肿胀度,HE染... 详细信息

目的研究萆薢总皂苷对大鼠急性痛风性关节炎的防治作用及机制。方法 Wistar大鼠,♂,72只,随机分组后,各用药组大鼠预先灌胃给予不同剂量萆薢总皂苷,随后右侧踝关节腔注射尿酸钠诱导急性痛风性关节炎。观察大鼠步态,测定关节肿胀度,HE染色进行病理学分析。ELISA法检测血清TNF-α、IL-1β、IL-18表达。Western blot法检测滑膜组织中pro-IL-1β、nalp3炎性体相关蛋白变化。结果萆薢总皂苷各浓度和秋水仙碱均可改善大鼠步态。TSD高、中剂量组与秋水仙碱类似,可降低大鼠关节肿胀度,病理学检查踝关节病变好转,血清TNF-α、IL-1β、IL-18明显减少,滑膜组织pro-IL-1β、nalp3、ASC、caspase-1前体和活性形式蛋白表达降低。结论萆薢总皂苷对大鼠急性痛风性关节炎具有防治作用,机制可能是抑制nalp3炎性体装配和激活,以及抑制炎性细胞因子的表达。

关键词：萆薢总皂苷急性痛风性关节炎尿酸钠 nalp3 炎性体炎性因子

nalp3表达与糖尿病肾病肾间质炎症的关系

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第三军医大学学报 2012年第10期34卷 959-962页

作者：张锦华张建国杨聚荣林利容詹俊李开龙何娅妮第三军医大学大坪医院野战外科研究所肾内科重庆400042

目的探讨糖尿病肾病(diabetic kidney disease,DKD)患者肾组织中nalp3的表达变化与肾小管间质炎症之间的关系。方法应用免疫组化及激光共聚焦技术检测DKD患者肾小管上皮细胞nalp3及IL-1β的表达变化及其相互关系,ELISA法检测尿液IL-1β... 详细信息

目的探讨糖尿病肾病(diabetic kidney disease,DKD)患者肾组织中nalp3的表达变化与肾小管间质炎症之间的关系。方法应用免疫组化及激光共聚焦技术检测DKD患者肾小管上皮细胞nalp3及IL-1β的表达变化及其相互关系,ELISA法检测尿液IL-1β水平,生化方法检测血清总胆固醇、低密度脂蛋白(LDL)、血肌酐(Serum creatinine,SCr)、24 h尿蛋白,计算出肾小球滤过率(estimated glomerular filtration rate,eGFR),对各指标与DKD时肾小管间质损伤、eGFR进行相关性分析。结果 DKD患者尿液IL-1β水平较对照组明显增高(Pnalp3及IL-1β的表达较对照组显著增高(Pnalp3表达增高的同时伴有IL-1β的增加;nalp3及IL-1β阳性细胞比例与患者年龄、体质量指数、舒张压、LDL、24 h尿蛋白、总胆固醇无显著相关性,但与血肌酐、尿IL-1β、eGFR显著相关(Pnalp3表达与炎性细胞因子IL-1β水平、肾间质损伤及肾功能改变明显相关,提示nalp3的表达变化很可能与DKD肾小管间质炎症反应存在密切关系。

关键词：糖尿病肾病 nalp3 IL-1β 炎症