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CP-25对大鼠胶原诱导性关节炎的治疗作用及对T细胞亚群的影响
类风湿关节炎(rheumatoid arthritis, RA)是一种慢性、系统性、自身免疫性疾病,其主要病理表现为增生性滑膜炎。RA疾病分布全球,其主要病理特征包括多种滑膜细胞增生、内衬层的增厚、炎性细胞浸润,软骨和骨...
汤小雨
关键词:胶原诱导性关节炎T细胞亚群
Specific role of synovial macrophages in rheumatoid arthritis
2017年
Rheumatoid arthritis(RA)is an autoimmune disease,which is characterized by synovial inflammation.Hyperplasia sublining macrophages found in synovium is an early hallmark of RA and effective treatment results in their diminution.However,the origin of these sublining macrophages in synovium(including infiltrated macrophages and tissue-resident macrophages)are still unknown both in animal models of arthritis and RA patients,let alone the differences and feature of these macrophages.In rheumatic synovium,macrophages are submitted to a large variety of micro-environmental signals which influence the phenotypic polarization and activation of macrophages.Understanding the mechanisms and functional consequences of the heterogeneous macrophages will contribute to confirm their potential role in synovial inflammation development.Furthermore,research on macrophage plasticity to soft-control their phenotypic polarization could lead to novel therapeutic approaches.
Xue-Zhi YANGYan CHANGWei WEI
关键词:POLARIZATIONHETEROGENEITY
Targeted inhibition of GRK2 kinase domain by CP-25 to reverse fibroblast-like synoviocytes dysfunction and improve collagen-induced arthritis in rats被引量:5
2021年
Rheumatoid arthritis(RA)is an autoimmune disease and is mainly characterized by abnormal proliferation of fibroblast-like synoviocytes(FLS).The up-regulated cellular membrane expression of G protein coupled receptor kinase 2(GRK2)of FLS plays a critical role in RA progression,the increase of GRK2 translocation activity promotes dysfunctional prostaglandin E4 receptor(EP4)signaling and FLS abnormal proliferation.Recently,although our group found that paeoniflorin-6’-O-benzene sulfonate(CP-25),a novel compound,could reverse FLS dysfunction via GRK2,little is known as to how GRK2 translocation activity is suppressed.Our findings revealed that GRK2 expression up-regulated and EP4 expression down-regulated in synovial tissues of RA patients and collagen-induced arthritis(CIA)rats,and prostaglandin E2(PGE2)level increased in arthritis.CP-25 could down-regulate GRK2 expression,up-regulate EP4 expression,and improve synovitis of CIA rats.CP-25 and GRK2 inhibitors(paroxetine or GSK180736 A)inhibited the abnormal proliferation of FLS in RA patients and CIA rats by down-regulating GRK2 translocation to EP4 receptor.The results of microscale thermophoresis(MST),cellular thermal shift assay,and inhibition of kinase activity assay indicated that CP-25 could directly target GRK2,increase the protein stability of GRK2 in cells,and inhibit GRK2 kinase activity.The docking of CP-25 and GRK2 suggested that the kinase domain of GRK2 might be an important active pocket for CP-25.G201,K220,K230,A321,and D335 in kinase domain of GRK2 might form hydrogen bonds with CP-25.Site-directed mutagenesis and co-immunoprecipitation assay further revealed that CP-25 down-regulated the interaction of GRK2 and EP4 via controlling the key amino acid residue of Ala321 of GRK2.Our data demonstrate that FLS proliferation is regulated by GRK2 translocation to EP4.Targeted inhibition of GRK2 kinase domain by CP-25 improves FLS function and represents an innovative drug for the treatment of RA by targeting GRK2.
Chenchen HanYifan LiYuwen ZhangYang WangDongqian CuiTingting LuoYu ZhangQian LiuHao LiChun WangDexiang XuYang MaWei Wei
CP-25抑制Th17细胞分化改善MRL/lpr狼疮小鼠肾损伤被引量:1
2021年
目的研究芍药苷-6’-O-苯磺酸酯(CP-25)对MRL/lpr狼疮小鼠的治疗作用及其对Th17细胞功能的调节。方法随机将MRL/lpr小鼠分为模型组、CP-25(20、40、80 mg·kg^(-1))组和泼尼松(prednisone,Pre)组(5 mg·kg^(-1)),设BALB/c小鼠为正常对照。给药组每日给予相应药物,正常组与模型组给予溶媒。HE染色观察小鼠肾脏病理,流式检测小鼠脾脏中T细胞亚群比例;Western blot和qPCR法分别检测小鼠脾脏p-STAT3、RORγt蛋白表达及IL-17A mRNA水平;ELISA法检测血清中IL-17A和抗dsDNA抗体水平。体外诱导Th17细胞分化,观察CP-25对Th17分化、p-STAT3和RORγt蛋白和IL-17A mRNA水平的影响。结果CP-25可明显改善MRL/lpr小鼠肾脏病理,降低抗dsDNA、IL-17A水平;降低小鼠脾脏中CD3^(+)细胞、CD4^(+)CD69^(+)细胞和CD4^(+)IL-17^(+)Th17细胞比例;降低脾脏p-STAT3、RORγt蛋白表达及IL-17A mRNA水平。体外结果显示,CP-25可抑制Th17细胞分化,降低p-STAT3、RORγt表达。结论CP-25可改善MRL/lpr小鼠肾脏病理,其机制与抑制STAT3的磷酸化,调节Th17细胞分化有关。
黄李娜王盛付王祥徐靓袁晓阳蒯佳婕魏伟严尚学
关键词:MRL/LPRTH17细胞STAT3RORΓT
Insulin-like growth factor-binding protein-3 inhibits IGF-1-induced proliferation of human hepatocellular carcinoma cells
2017年
OBJECTIVE Basic fibroblast growth factor(b FGF)and platelet-derived growth factor(PDGF)produced by hepatocellular carcinoma(HCC)cells are responsible for the cell growth.Accumulating evidence shows that insulin-like growth factor-binding protein-3(IGFBP-3)suppresses HCC cell proliferation in both IGF-dependent and independent manners.The present study is to investigate whether treatment with exogenous IGFBP-3 inhibits bF GF and PDGF production and the cell proliferation of HCC cells.METHODS Cell Counting Kit 8 assay were designed to detect HCC cell proliferation,transcription factor early growth response-1(EGR1)involving in IGFBP-3 regulation of b FGF and PDGF were detected by RT-PCR and Western blot assays.Western blot assay was adopted to detect the IGFBP-3 regulating insulin-like growth factor 1 receptor(IGF-1R)signaling pathway.RESULTS The present study demonstrates that IGFBP-3 suppressed IGF-1-induced b FGF and PDGF expression while it does not affect their expression in the absence of IGF-1.To delineate the underlying mechanism,Western-blot and RT-PCR assays confirmed that the transcription factor early growth response protein 1(EGR1)is involved in IGFBP-3 regulation of b FGF and PDGF.IGFBP-3 inhibition of type 1 insulin-like growth factor receptor(IGF1R),ERK and AKT activation is IGF-1-dependent.Furthermore,transient transfection with constitutively activated AKT or MEK partially blocks the IGFBP-3 inhibition of EGR1,b FGF and PDGF expression.CONCLUSION In conclusion,these findings suggest that IGFBP-3suppresses transcription of EGR1 and its target genes b FGF and PDGF through inhibiting IGF-1-dependent ERK and AKT activation.It demonstrates the importance of IGFBP-3 in the regulation of HCC cell proliferation,suggesting that IGFBP-3 could be a target for the treatment of HCC.
Yang MAChen-chen HANYi-fan LIYang WANGWei WEI
A novel anti-inflammatory and immunomodulatory drug CP-25 alleviated collagen induced arthritis by down-regulating BAFF-NF-κκB signaling pathway
2017年
OBJECTIVE To investigated the regulatory effect of paeoniflorin-6′-O-benzene sulfonate(CP-25) on B cell activating factor(BAFF)/BAFF receptor-nuclear factor of kappa B(NF-κB) signaling in B cell of collagen induced-arthritis(CIA) mice.METHODS Mice CIA was induced by injection of typeⅡcollagen(CⅡ).The arthritis index(AI) and swollen joint count(SJC) were assessed,and histopathology of spleen and joints were observed.The percentage of B cells subsets,BAFF receptor expressions were analyzed by flow cytometry.BAFF and immunoglobulin(Ig) levels were measured by protein antibody array.The expressions of TRAF2,MKK3,MKK6,p-P38,and p-NF-κB65 in NF-κB signaling mediated by BAFF were analyzed by western blot.RESULTS CP-25 decreased AI and SJC,restored abnormal weights,reduced thymus index and spleen index,inhibited T/B cells proliferation,alleviated the histopathology of spleen and joints in CIA mice.CP-25 also reduced high levels of serum BAFF and immunoglobulin,decreased CD19+B cells,CD19+CD27+B cells,and CD19-CD27+CD138+plasma cells,inhibited BAFFR and TACI expressions,decreased the expressions of TRAF2,MKK3,MKK6,p-P38,and p-NF-κB65.Compared with biological agents etanercept and rituximab,CP-25 restored high T cells proliferation and percentages of B subsets to normal level,and recovered the high levels of IgA,IgD,IgG1,IgG2 a and high expressions molecules in NF-κB signaling to normal levels.The action intensity of rituximab and etanercept was more strong than CP-25.The inhibitor effects of rituximab and etanercept on AI and SJC,thymus index,proliferation of T cells and B cells subsets were strong,and down-regulated the indexes to under normal levels.CONCLUSION CP-25 might be a promising anti-inflammatory immune and regulation drug,which alleviated CIA and regulated the functions of B cells through BAFF/BAFF receptor-NF-κB signaling.
Jin-ling SHUXian-zheng ZHANGLe HANFeng ZHANGYu-jing WUXiao-yu TangChen WANGYu TAIQing-tong WANGJing-yu CHENLing-ling ZHANGWei WEI
关键词:BAFF
G protein coupled receptors signaling pathways implicate in inflammatory and immune response of rheumatoid arthritis被引量:4
2017年
G protein coupled receptors(GPCRs)are transmembrane receptor proteins,which allow signals to transfer across membrane.GPCRs include a large number of receptors,different receptors mediated different signaling pathways of GPCRs-adenylyl cyclase(AC)-cyclic adenosine 3',5'-monophosphate(c AMP),including β2 adrenergic receptors(β2-ARs)-AC-c AMP signaling pathways,E-prostanoid2/4(EP2/4)-AC-cA MP signaling pathways.Regulatory proteins,such as G protein coupled receptor kinases(GRKs)andβ-arrestins,play important modulatory roles in GPCRs signaling pathway.GPCRs signaling pathway and regulatory proteins implicate the pathogenesis process of inflammatory and immune response.Rheumatoid arthritis(RA)is an autoimmune disease characterized by synovitis and accompanied with inflammatory and abnormal immune response.This article review the advances on GPCRs signaling pathway implicating in the inflammatory and immune response of RA.
Jin-ling SHUFeng ZHANGLing-ling ZHANGWei WEI
关键词:GPCRS
IL-6下调腺苷A3受体信号促进胶原性关节炎大鼠Thl7细胞分化的机制研究
类风湿关节炎(RA)是一种常见的慢性自身免疫病,滑膜组织为RA的主要炎症靶点,大量炎性细胞浸润到滑膜组织,并产生多种致炎性细胞因子,如白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)、IL-6、IL-17等...
胡珊珊
关键词:白介素6
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PGE2通过EP4/cAMP/PKA信号通路调控成纤维样滑膜细胞OAT1的表达及CP--25的作用
有机阴离子转运蛋白(organic anion transporters, OATs)是由超过10种跨膜转运蛋白所组成,是溶质载体超家族中的重要一员,其代表转运蛋白有 OAT1、OAT2和 OAT3等。有机阴离子转运蛋白...
王斌
关键词:胶原性关节炎滑膜细胞有机阴离子转运蛋白
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抗IgD抗体及在自身免疫病中的作用被引量:1
2015年
抗免疫球蛋白D抗体(anti-immunoglobulin D antibody,抗IgD抗体)一直以来主要作为工具药来研究正常B细胞上的膜结合型IgD(membrane IgD,m IgD)。最新研究表明,在病理状态下,抗IgD抗体可以通过选择性清除成熟B细胞、降低自身抗体的水平、抑制B细胞上B细胞活化因子(B cell activating factor belonging to the TNF family,BAFF)的过多表达等来影响自身免疫病的进程。通过抗IgD抗体的治疗,能明显缓解类风湿关节炎(rheumatoid arthritis,RA)、系统性红斑狼疮(systemic lupus erythematosus,SLE)等模型小鼠的病变。抗IgD抗体的研究不断深入,将为其作为研究治疗自身免疫病的靶点提供新思路。本文就抗IgD抗体的免疫学功能和在自身免疫病中的相关作用的研究进展做一综述。
陈恒石吴育晶黄琼陈文生魏伟
关键词:B细胞自身抗体自身免疫病
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