期刊文献+
共找到6,651篇文章
< 1 2 250 >
每页显示 20 50 100
African swine fever virus MGF505-3R inhibits cGAS-STING-mediated IFN-βpathway activation by degrading TBK1 被引量:1
1
作者 Mingyang Cheng Jiawei Luo +14 位作者 Yuetong Duan Yu Yang Chunwei Shi Yu Sun Yiyuan Lu Junhong Wang Xiaoxu Li Jianzhong Wang Nan Wang Wentao Yang Yanlong Jiang Guilian Yang Yan Zeng Chunfeng Wang Xin Cao 《Animal Diseases》 2022年第3期154-164,共11页
African swine fever virus(ASFV)is an important pathogen causing acute infectious disease in domestic pigs and wild boars that seriously endangers the global swine industry.As ASFV is structurally complex and encodes a... African swine fever virus(ASFV)is an important pathogen causing acute infectious disease in domestic pigs and wild boars that seriously endangers the global swine industry.As ASFV is structurally complex and encodes a large number of functional proteins,no effective vaccine has been developed to date.Thus,dissecting the mechanisms of immune escape induced by ASFV proteins is crucial.A previous study showed that the ASFV-encoded protein is an important factor in host immunity.In this study,we identified a negative regulator,MGF505-3R,that significantly downregulated cGAS/STING-and poly(dG:dC)-mediated IFN-βand interferon stimulation response element(ISRE)reporter activity and suppressed IFNB1 and IFIT2 mRNA levels.In addition,TBK1,IRF3 and IκBαphosphorylation levels were also inhibited.Mechanistically,MGF505-3R interacted with cGAS/TBK1/IRF3 and targeted TBK1 for degradation,thereby disrupting the cGAS-STING-mediated IFN-βsignaling pathway,which appears to be highly correlated with autophagy.Knockdown MGF505-3R expression enhanced IFN-βand IL-1βproduction.Taken together,our study revealed a negative regulatory mechanism involving the MGF505-3R-cGAS-STING axis and provided insights into an evasion strategy employed by ASFV that involves autophagy and innate signaling pathways. 展开更多
关键词 African swine fever virus MGF505-3R cGAS/STING signaling pathway TBK1 Innate immunity
下载PDF
IFN-β通过STAT1诱导SARI表达抑制AML细胞增殖并促进凋亡
2
作者 林艳凤 洪小颖 +4 位作者 黄莹莹 王小花 吴玮 林东红 薛龑 《中国免疫学杂志》 CAS CSCD 北大核心 2024年第6期1137-1141,共5页
目的:探讨IFN-β诱导SARI表达对急性粒细胞性白血病(AML)细胞增殖、凋亡的作用,并筛选其潜在的调控分子。方法:qPCR、Western blot筛选SARI低表达的AML细胞作为实验细胞株;不同浓度IFN-β干预AML细胞,于不同时间采用qPCR、Western blot... 目的:探讨IFN-β诱导SARI表达对急性粒细胞性白血病(AML)细胞增殖、凋亡的作用,并筛选其潜在的调控分子。方法:qPCR、Western blot筛选SARI低表达的AML细胞作为实验细胞株;不同浓度IFN-β干预AML细胞,于不同时间采用qPCR、Western blot检测SARI表达,选取IFN-β作用的适当浓度和时间;采用RNA-Seq转录组测序及KEGG富集分析初步筛选IFN-β诱导AML细胞SARI表达的潜在调控分子;通过相应分子抑制剂联合IFN-β处理AML细胞,MTS法检测细胞增殖,流式细胞术检测细胞凋亡;明确该分子参与IFN-β诱导SARI表达对AML细胞增殖及凋亡的作用。结果:HL60和NB4细胞SARI表达相对较低,选为实验细胞株;1 ng/ml IFN-β作用12 h后AML细胞SARI表达升高且细胞增殖被抑制,凋亡增多;筛选STAT1为IFN-β诱导SARI表达的潜在调控分子;抑制STAT1后,IFN-β对AML细胞SARI表达、增殖抑制、凋亡促进的作用被明显逆转。结论:IFN-β可通过STAT1诱导AML细胞SARI表达,抑制细胞增殖,促进细胞凋亡。 展开更多
关键词 ifn-β SARI STAT1 AML 增殖 凋亡
下载PDF
结核分枝杆菌特异性IFN-γ、IL-2联合检测在肺结核与细菌性肺炎鉴别诊断中的应用
3
作者 许静 王伟 李团团 《中国感染控制杂志》 CAS CSCD 北大核心 2024年第9期1173-1177,共5页
目的评价结核分枝杆菌特异性细胞因子干扰素-γ(IFN-γ)、白细胞介素-2(IL-2)双因子联合检测在肺结核与细菌性肺炎鉴别诊断中的应用价值。方法选择阜阳市人民医院2022年1月-2023年10月呼吸科住院患者91例,明确诊断为肺结核患者45例(肺... 目的评价结核分枝杆菌特异性细胞因子干扰素-γ(IFN-γ)、白细胞介素-2(IL-2)双因子联合检测在肺结核与细菌性肺炎鉴别诊断中的应用价值。方法选择阜阳市人民医院2022年1月-2023年10月呼吸科住院患者91例,明确诊断为肺结核患者45例(肺结核组)和细菌性肺炎患者46例(肺炎组),均进行双因子联合检测,比对分析双因子联合检测与C反应蛋白(CRP)对肺结核和细菌性肺炎鉴别诊断的效果。结果使用双因子联合检测对肺结核与细菌性肺炎进行鉴别诊断,灵敏度为86.7%、特异度为84.8%,受试者工作特征曲线下面积(AUC)值为0.928(95%CI:0.870~0.986),与CRP的鉴别诊断效果相比差异有统计学意义(P<0.05)。结论结核分枝杆菌特异性细胞因子IFN-γ、IL-2联合检测在鉴别肺结核与细菌性肺炎时具有较高的应用价值,能为临床肺结核和细菌性肺炎的鉴别诊断提供依据。 展开更多
关键词 肺结核 细菌性肺炎 ifn-Γ IL-2 联合检测 鉴别诊断
下载PDF
藏獒IFN-γ基因在毕赤酵母中的表达与抗病毒活性分析
4
作者 宋世斌 何小兵 +1 位作者 景志忠 陈国华 《中兽医医药杂志》 CAS 2024年第5期1-6,共6页
采用毕赤酵母表达系统表达藏獒γ-干扰素(Tibetan mastiff interferon gamma,TmIFN-γ)并分析其生物活性,为抗病毒生物制品的研发与临床应用奠定基础。将构建的TmIFN-γ的真核表达质粒pPIC9k-TmIFN-γ转化至毕赤酵母GS115细胞,用不同浓... 采用毕赤酵母表达系统表达藏獒γ-干扰素(Tibetan mastiff interferon gamma,TmIFN-γ)并分析其生物活性,为抗病毒生物制品的研发与临床应用奠定基础。将构建的TmIFN-γ的真核表达质粒pPIC9k-TmIFN-γ转化至毕赤酵母GS115细胞,用不同浓度的G418筛选得到多拷贝重组菌株;利用甲醇进行诱导表达,以镍层析柱纯化目的蛋白,对表达产物进行SDS-PAGE和Western blotting鉴定;通过CCK-8试验检测重组TmIFN-γ蛋白的细胞毒性作用,利用VSV-MDBK系统检测其抗病毒生物活性。结果显示,成功筛选得到高拷贝pPIC9k-TmIFN-γ重组转化毕赤酵母菌株,利用甲醇诱导可获得TmIFN-γ重组蛋白,该蛋白对细胞无毒性,具有显著抗病毒活性,其抗病毒生物效价为1.727×10~5IU/mL。本研究获得了具有抗病毒活性的TmIFN-γ,有助于进一步探索TmIFN-γ的功能和开发新型基因工程抗病毒药物。 展开更多
关键词 藏獒ifn-γ 酵母表达 抗病毒活性
下载PDF
血清RAGE、HMGB1水平与重症肺炎急性呼吸窘迫综合征发病及IFN-γ/IL-4变化的关系 被引量:2
5
作者 王敬才 郭春艳 +1 位作者 杨丽昕 敬小青 《实用医学杂志》 CAS 北大核心 2024年第4期515-520,共6页
目的探究血清晚期糖基化终产物受体(RAGE)、高迁移率族蛋白B1(high mobility group protein B1,HMGB1)水平与重症肺炎(SP)急性呼吸窘迫综合征(ARDS)发病及γ-干扰素(IFN-γ)/白细胞介素4(IL-4)变化的关系。方法前瞻性选取2020年3月至202... 目的探究血清晚期糖基化终产物受体(RAGE)、高迁移率族蛋白B1(high mobility group protein B1,HMGB1)水平与重症肺炎(SP)急性呼吸窘迫综合征(ARDS)发病及γ-干扰素(IFN-γ)/白细胞介素4(IL-4)变化的关系。方法前瞻性选取2020年3月至2022年2月我院收治的100例SP患儿为研究对象,根据患儿是否发生继发性ARDS将患儿分为ARDS组(n=56)和对照组(n=44),收集患儿一般资料,采集外周血以酶联免疫吸附法进行RAGE、HMGB1、IFN-γ和IL-4表达水平检测,采用多因素logistic回归分析SP患儿继发ARDS的影响因素,采用Pearson相关性分析其与IFN-γ/IL-4的相关性,并采用受试者工作曲线(ROC)分析RAGE、HMGB1表达对SP患儿继发ARDS的预测价值。结果两组SP患儿性别、年龄、体温以及发病季节之间无显著差异,ARDS组致病菌种类多于对照组,PaO_(2)/FiO_(2)和APS评分、血清RAGE、HMGB1、IFN-γ和IL-4表达水平以及IFN-γ/IL-4比值均高于对照组(P<0.05)。经多因素logistic回归分析可知,致病菌种类、PaO_(2)/FiO_(2)、RAGE、HMGB1表达、IFN-γ、IL-4和IFN-γ/IL-4均为SP患儿继发ARDS的影响因素。经Pearson相关检验,SP患儿血清RAGE、HMGB1表达水平与IFN-γ、IL-4和IFN-γ/IL-4均呈正相关(P<0.05)。经ROC曲线分析可得,血清RAGE、HMGB1水平预测SP患儿发生ARDS的AUC分别为0.707和0.750,灵敏度分别为73.2%、64.3%,特异度分别为68.2%、77.3%,两者联合预测的AUC为0.848,灵敏度和特异度分别为80.4%和81.8%。结论SP继发ARDS患儿血清中RAGE、HMGB1表达水平较高,与IFN-γ/IL-4呈正相关,监测患儿血清RAGE、HMGB1表达对SP患儿继发ARDS的风险有一定的预测价值。 展开更多
关键词 晚期糖基化终产物受体 高迁移率族蛋白B1 重症肺炎 急性呼吸窘迫综合征 ifn-Γ IL-4
下载PDF
高脂肪饮食促进TLR2的表达促进3T3L1脂肪细胞分泌IFN-γ诱导胰岛素抵抗的发生及发展
6
作者 白继昌 谈力欣 +2 位作者 刘赞朝 杨洋 朱亚军 《河北医学》 CAS 2024年第3期405-411,共7页
目的:探讨高脂饮食诱导胰岛素抵抗的机制,以及了解高脂饮食诱导胰岛素抵抗的脂肪细胞的表型变化。方法:雄性C57 BL/6 J小鼠,给予正常饮食和高脂饮食。从正常饮食或高脂饮食喂养2周的小鼠中分离附睾脂肪组织。实时荧光定量RT-PCR检测γ-... 目的:探讨高脂饮食诱导胰岛素抵抗的机制,以及了解高脂饮食诱导胰岛素抵抗的脂肪细胞的表型变化。方法:雄性C57 BL/6 J小鼠,给予正常饮食和高脂饮食。从正常饮食或高脂饮食喂养2周的小鼠中分离附睾脂肪组织。实时荧光定量RT-PCR检测γ-干扰素(Interferonγ,IFN-γ)和toll样受体2(toll-like receptor 2,TLR2)mRNA的表达。流式细胞术来检测表达TLR2或IFN-γ的脂肪细胞的数量。苏木精-伊红染色分析胰腺组织。免疫组化分析脂肪组织中TLR2和IFN-γ的表达。FFA或Zymosan A处理3T3-L1脂肪细胞,并通过实时荧光定量RT-PCR检测IFN-γ和TLR2 mRNA的表达。结果:对脂肪细胞中基因表达谱的分析表明,高脂肪摄入诱导了IFN-γ和TLR2的表达提高。流式细胞术分析显示存在共表达TLR2和IFN-γ的脂肪细胞(TLR2/IFN-γ脂肪细胞),与皮下脂肪组织相比,高脂肪摄入增加了内脏脂肪组织中TLR2/IFN-γ脂肪细胞的数量。游离脂肪酸通过TLR2信号增加3T3-L1脂肪细胞中IFN-γ的表达。结论:TLR2/IFN-γ脂肪细胞可能通过诱导内脏脂肪组织IFN-γ的表达,参与高脂诱导的胰岛素抵抗的发生。 展开更多
关键词 TLR2 脂肪细胞 ifn-Γ 胰岛素抵抗
下载PDF
茶花鸡2号IFN-α基因克隆及生物信息学分析
7
作者 刘琛 何永江 +5 位作者 豆腾飞 杨明华 潘洪彬 赵素梅 李永能 黄英 《中国畜牧杂志》 CAS CSCD 北大核心 2024年第1期217-222,共6页
本研究旨在克隆茶花鸡2号α干扰素基因(IFN-α)CDS区序列并进行生物信息学分析,为后续研究IFN-α基因对茶花鸡2号免疫功能的影响提供参考。以茶花鸡2号为实验对象设计IFN-α引物,提取总RNA,反转录PCR扩增并克隆其编码区序列,进行生物信... 本研究旨在克隆茶花鸡2号α干扰素基因(IFN-α)CDS区序列并进行生物信息学分析,为后续研究IFN-α基因对茶花鸡2号免疫功能的影响提供参考。以茶花鸡2号为实验对象设计IFN-α引物,提取总RNA,反转录PCR扩增并克隆其编码区序列,进行生物信息学分析。结果显示茶花鸡2号IFN-α基因CDS序列全长582 bp,IFN-α蛋白等电点5.05,平均疏水指数-0.514,为酸性亲水蛋白,且存在信号肽和1个跨膜区,主要定位于细胞核。IFN-α蛋白被4个N糖基化位点、5个O糖基化位点和20个磷酸化位点修饰,主要由α-螺旋与无规卷曲构成。茶花鸡2号与固始鸡、海兰鸡、惠阳胡须鸡、罗曼鸡和乌骨鸡的氨基酸同源性分别为95.9%、97.9%、97.9%、97.9%和95.9%。IFN-α蛋白与IRF7、IFNAR1、IFNAR2和IFNK等蛋白存在互作关系。本研究结果可为进一步探讨IFN-α基因在茶花鸡2号病毒疾病防治中的作用提供理论依据。 展开更多
关键词 茶花鸡2号 ifn-α基因 基因克隆 生物信息学分析
下载PDF
血红素加氧酶-1通过诱导抗病毒蛋白的表达增强IFN-α抗HBV效应
8
作者 笪蔚 王琴 +4 位作者 魏安邦 张浩 汪任冰 刘倩 周强 《安徽医科大学学报》 CAS 北大核心 2024年第2期324-330,共7页
目的探讨血红素加氧酶-1(HO-1)对HBV复制的作用及HO-1联合α-干扰素(IFN-α)的抗病毒效应。方法以HepG2.2.15细胞和HBV 1.3质粒转染HepG2细胞即HepG2-HBV1.3为HBV复制细胞模型;血红素(Hemin)分别处理HepG2.2.15和HepG2-HBV1.3细胞,诱导H... 目的探讨血红素加氧酶-1(HO-1)对HBV复制的作用及HO-1联合α-干扰素(IFN-α)的抗病毒效应。方法以HepG2.2.15细胞和HBV 1.3质粒转染HepG2细胞即HepG2-HBV1.3为HBV复制细胞模型;血红素(Hemin)分别处理HepG2.2.15和HepG2-HBV1.3细胞,诱导HO-1表达;CCK-8评估Hemin对HepG2、HepG2.2.15的毒性作用;化学发光法分析Hemin处理组及si-HO-1等实验组上清液中HBsAg、HBeAg;RT-qPCR分析HO-1、IFN-β、HBV-DNA;Western blot分析IRF-3、JAK/STAT信号通路中相关分子的表达;Hemin联合IFN-α处理HepG2.2.15,监测HO-1是否具有协同IFN-α抗病毒效应。结果Hemin剂量依赖性诱导HO-1,HO-1被诱导后发挥显著的抗HBV效应,同时IFN-β、IRF-3及JAK/STAT信号通路中IRF-9、MxA的表达均增加。沉默HO-1表达能逆转Hemin诱导组的抗病毒效应,同时I型干扰素IFN-β也呈现低表达,JAK/STAT信号通路中的IRF-9、MxA的表达也被抑制。Hemin联合IFN-α发挥更强的抗病毒作用。结论HO-1能够发挥抗HBV效应,这种效应可能是增加IRF-3的磷酸化诱导I型干扰素表达来激活JAK/STAT信号通路发挥抗病毒效应;HO-1可以协同IFN-α发挥抗病毒作用。 展开更多
关键词 血红素 血红素加氧酶-1 JAK/STAT ifn-β
下载PDF
IFN-α抗病毒治疗118例慢性乙型肝炎并10年随访分析
9
作者 龙林 吴志国 +5 位作者 周瑶 向海鸿 邱芳 罗小露 刘翠芸 孙水林 《南昌大学学报(医学版)》 2024年第3期6-10,37,共6页
目的 探讨IFN-α抗病毒治疗慢性乙型肝炎(CHB)患者的效果,为CHB的抗病毒治疗提供参考。方法选取接受普通IFN-α治疗且资料完整的CHB患者118例,通过门诊定期复诊和电话随诊收集患者的乙肝五项[乙型肝炎表面抗原(HBsAg)、乙型肝炎表面抗体... 目的 探讨IFN-α抗病毒治疗慢性乙型肝炎(CHB)患者的效果,为CHB的抗病毒治疗提供参考。方法选取接受普通IFN-α治疗且资料完整的CHB患者118例,通过门诊定期复诊和电话随诊收集患者的乙肝五项[乙型肝炎表面抗原(HBsAg)、乙型肝炎表面抗体(HBsAb)、乙型肝炎e抗原(HBeAg)、乙型肝炎e抗体(HBeAb)、乙型肝炎核心抗体(HBcAb)]、乙肝DNA定量(HBV-DNA)和谷丙转氨酶(ALT)水平。比较治疗前后、随访期间不同时间点的HBV-DNA和HBsAg阴转率、HBeAg/HBeAb血清转换率和ALT复常率等。结果 HBV-DNA阴转率及HBsAg阴转率随治疗时间的延长而提高,HBV-DNA阴转率在治疗第24、36、48周时的阴转率明显高于第12周,HBsAg阴转率在治疗第48周明显高于第12周和24周,差异均有统计学意义(P<0.05)。停药后第24~432周各随访节点HBV-DNA阴转率及HBsAg阴转率呈先降后趋于稳定的趋势。HBeAg/HBeAb血清转换率随治疗时间的延长而升高,治疗第48周其转换率明显高于第12周(P<0.05);HBeAg/HBeAb血清转换率及SVR随停药时间的延长呈先降后趋于稳定的趋势。停药后,HBeAg/HBeAb血清转换率在各随访节点差异均无统计学意义(P>0.05)。病毒学复发率停药后先上升,在停药第144周呈现稳定趋势。ALT复常率在停药第144周呈现稳定趋势,停药第144周的ALT复常率明显高于停药第12周(P<0.05)。结论 IFN-α抗病毒治疗CHB可取得较好的疗效,在治疗及停药后各随访节点,HBV-DNA阴转率、HBsAg阴转率、ALT复常率、HBeAg/HBeAb转换率均可获得较高的应答率。 展开更多
关键词 慢性乙型肝炎 抗病毒治疗 ifn-Α 疗效
下载PDF
Cell metabolism pathways involved in the pathophysiological changes of diabetic peripheral neuropathy 被引量:5
10
作者 Yaowei Lv Xiangyun Yao +3 位作者 Xiao Li Yuanming Ouyang Cunyi Fan Yun Qian 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第3期598-605,共8页
Diabetic peripheral neuropathy is a common complication of diabetes mellitus.Elucidating the pathophysiological metabolic mechanism impels the generation of ideal therapies.However,existing limited treatments for diab... Diabetic peripheral neuropathy is a common complication of diabetes mellitus.Elucidating the pathophysiological metabolic mechanism impels the generation of ideal therapies.However,existing limited treatments for diabetic peripheral neuropathy expose the urgent need for cell metabolism research.Given the lack of comprehensive understanding of energy metabolism changes and related signaling pathways in diabetic peripheral neuropathy,it is essential to explore energy changes and metabolic changes in diabetic peripheral neuropathy to develop suitable treatment methods.This review summarizes the pathophysiological mechanism of diabetic peripheral neuropathy from the perspective of cellular metabolism and the specific interventions for different metabolic pathways to develop effective treatment methods.Various metabolic mechanisms(e.g.,polyol,hexosamine,protein kinase C pathway)are associated with diabetic peripheral neuropathy,and researchers are looking for more effective treatments through these pathways. 展开更多
关键词 cell metabolism diabetic peripheral neuropathy peripheral nerve injury protein kinase C pathway reactive oxygen species.
下载PDF
Calculus bovis inhibits M2 tumor-associated macrophage polarization via Wnt/β-catenin pathway modulation to suppress liver cancer 被引量:6
11
作者 Zhen Huang Fan-Ying Meng +12 位作者 Lin-Zhu Lu Qian-Qian Guo Chang-Jun Lv Nian-Hua Tan Zhe Deng Jun-Yi Chen Zi-Shu Zhang Bo Zou Hong-Ping Long Qing Zhou Sha Tian Si Mei Xue-Fei Tian 《World Journal of Gastroenterology》 SCIE CAS 2024年第29期3511-3533,共23页
BACKGROUND Calculus bovis(CB),used in traditional Chinese medicine,exhibits anti-tumor effects in various cancer models.It also constitutes an integral component of a compound formulation known as Pien Tze Huang,which... BACKGROUND Calculus bovis(CB),used in traditional Chinese medicine,exhibits anti-tumor effects in various cancer models.It also constitutes an integral component of a compound formulation known as Pien Tze Huang,which is indicated for the treatment of liver cancer.However,its impact on the liver cancer tumor microenvironment,particularly on tumor-associated macrophages(TAMs),is not well understood.AIM To elucidate the anti-liver cancer effect of CB by inhibiting M2-TAM polarization via Wnt/β-catenin pathway modulation.METHODS This study identified the active components of CB using UPLC-Q-TOF-MS,evaluated its anti-neoplastic effects in a nude mouse model,and elucidated the underlying mechanisms via network pharmacology,transcriptomics,and molecular docking.In vitro assays were used to investigate the effects of CB-containing serum on HepG2 cells and M2-TAMs,and Wnt pathway modulation was validated by real-time reverse transcriptase-polymerase chain reaction and Western blot analysis.RESULTS This study identified 22 active components in CB,11 of which were detected in the bloodstream.Preclinical investigations have demonstrated the ability of CB to effectively inhibit liver tumor growth.An integrated approach employing network pharmacology,transcriptomics,and molecular docking implicated the Wnt signaling pathway as a target of the antineoplastic activity of CB by suppressing M2-TAM polarization.In vitro and in vivo experiments further confirmed that CB significantly hinders M2-TAM polarization and suppresses Wnt/β-catenin pathway activation.The inhibitory effect of CB on M2-TAMs was reversed when treated with the Wnt agonist SKL2001,confirming its pathway specificity.CONCLUSION This study demonstrated that CB mediates inhibition of M2-TAM polarization through the Wnt/β-catenin pathway,contributing to the suppression of liver cancer growth. 展开更多
关键词 Calculus bovis M2 tumor-associated macrophage polarization Liver cancer Wnt/β-catenin pathway Tumor microenvironment
下载PDF
Timosaponin AⅢ induces drug-metabolizing enzymes by activating constitutive androstane receptor (CAR) via dephosphorylation of the EGFR signaling pathway 被引量:1
12
作者 Muhammad Zubair Hafiz Jie Pan +4 位作者 Zhiwei Gao Ying Huo Haobin Wang Wei Liu Jian Yang 《Journal of Biomedical Research》 CAS CSCD 2024年第4期382-396,共15页
The current study aimed to assess the effect of timosaponin AⅢ(T-AⅢ)on drug-metabolizing enzymes during anticancer therapy.The in vivo experiments were conducted on nude and ICR mice.Following a 24-day administratio... The current study aimed to assess the effect of timosaponin AⅢ(T-AⅢ)on drug-metabolizing enzymes during anticancer therapy.The in vivo experiments were conducted on nude and ICR mice.Following a 24-day administration of T-AⅢ,the nude mice exhibited an induction of CYP2B10,MDR1,and CYP3A11 expression in the liver tissues.In the ICR mice,the expression levels of CYP2B10 and MDR1 increased after a three-day T-AⅢ administration.The in vitro assessments with HepG2 cells revealed that T-AⅢ induced the expression of CYP2B6,MDR1,and CYP3A4,along with constitutive androstane receptor(CAR)activation.Treatment with CAR siRNA reversed the T-AⅢ-induced increases in CYP2B6 and CYP3A4 expression.Furthermore,other CAR target genes also showed a significant increase in the expression.The up-regulation of murine CAR was observed in the liver tissues of both nude and ICR mice.Subsequent findings demonstrated that T-AⅢ activated CAR by inhibiting ERK1/2 phosphorylation,with this effect being partially reversed by the ERK activator t-BHQ.Inhibition of the ERK1/2 signaling pathway was also observed in vivo.Additionally,T-AⅢ inhibited the phosphorylation of EGFR at Tyr1173 and Tyr845,and suppressed EGF-induced phosphorylation of EGFR,ERK,and CAR.In the nude mice,T-AⅢ also inhibited EGFR phosphorylation.These results collectively indicate that T-AⅢ is a novel CAR activator through inhibition of the EGFR pathway. 展开更多
关键词 timosaponin AⅢ CAR metabolism enzyme ERK1/2 signaling pathway EGFR signaling pathway
下载PDF
Enterogenic Stenotrophomonas maltophilia migrates to the mammary gland to induce mastitis by activating the calcium-ROS-AMPK-mTOR-autophagy pathway 被引量:1
13
作者 Zhaoqi He Caijun Zhao +7 位作者 Yuhong He Zhuoyu Liu Guyue Fan Kun Zhu Yiqi Wang Naisheng Zhang Yunhe Fu Xiaoyu Hu 《Journal of Animal Science and Biotechnology》 SCIE CAS CSCD 2024年第1期236-252,共17页
Background Mastitis is an inflammatory disease of the mammary gland that has serious economic impacts on the dairy industry and endangers food safety.Our previous study found that the body has a gut/rumen-mammary glan... Background Mastitis is an inflammatory disease of the mammary gland that has serious economic impacts on the dairy industry and endangers food safety.Our previous study found that the body has a gut/rumen-mammary gland axis and that disturbance of the gut/rumen microbiota could result in‘gastroenterogenic mastitis'.However,the mechanism has not been fully clarified.Recently,we found that long-term feeding of a high-concentrate diet induced mastitis in dairy cows,and the abundance of Stenotrophomonas maltophilia(S.maltophilia)was significantly increased in both the rumen and milk microbiota.Accordingly,we hypothesized that‘gastroenterogenic mastitis'can be induced by the migration of endogenous gut bacteria to the mammary gland.Therefore,this study investigated the mechanism by which enterogenic S.maltophilia induces mastitis.Results First,S.maltophilia was labelled with superfolder GFP and administered to mice via gavage.The results showed that treatment with S.maltophilia promoted the occurrence of mastitis and increased the permeability of the blood-milk barrier,leading to intestinal inflammation and intestinal leakage.Furthermore,tracking of ingested S.maltophilia revealed that S.maltophilia could migrate from the gut to the mammary gland and induce mastitis.Subsequently,mammary gland transcriptome analysis showed that the calcium and AMPK signalling pathways were significantly upregulated in mice treated with S.maltophilia.Then,using mouse mammary epithelial cells(MMECs),we verified that S.maltophilia induces mastitis through activation of the calcium-ROS-AMPK-mTOR-autophagy pathway.Conclusions In conclusion,the results showed that enterogenic S.maltophilia could migrate from the gut to the mammary gland via the gut-mammary axis and activate the calcium-ROS-AMPK-mTOR-autophagy pathway to induce mastitis.Targeting the gut-mammary gland axis may also be an effective method to treat mastitis. 展开更多
关键词 Calcium-ROS-AMPK-mTOR-autophagy pathway Gut-mammary axis MASTITIS S.maltophilia
下载PDF
IFN-γ联合IL-6在菌阴性肺结核诊断中的应用分析
14
作者 刘轩妙 徐俊驰 +1 位作者 岳晓冬 胥萍 《标记免疫分析与临床》 CAS 2024年第3期450-455,475,共7页
目的探讨IFN-γ联合IL-6在菌阴性肺结核临床诊断中的应用及其临床意义。方法收集2021年10月21日至2023年4月27日期间在苏州大学附属传染病医院病例266例。依据肺结核诊断标准(WS288-2017),肺结核患者196例,其中男性130例,女性66例,平均... 目的探讨IFN-γ联合IL-6在菌阴性肺结核临床诊断中的应用及其临床意义。方法收集2021年10月21日至2023年4月27日期间在苏州大学附属传染病医院病例266例。依据肺结核诊断标准(WS288-2017),肺结核患者196例,其中男性130例,女性66例,平均年龄58.4±17.1岁;病灶双侧患者141例,病灶单侧患者55例;菌阳患者92例,菌阴患者104例。职业性尘肺病患者70例,其中男性69例,女性1例,平均年龄62.7±8.9岁。健康对照组20例,其中男性10例,女性10例,平均年龄58.6±6.3岁。采用流式细胞术检测血浆中细胞因子IFN-γ、IFN-α、IL-2、IL-4、IL-5、IL-6、IL-8、TNF-α、IL-10、IL-12P70、IL-1β、IL-17的表达水平,比较不同组别中这12项炎症细胞因子的差异。结果(1)活动性肺结核患者组血浆IFN-γ、IL-6水平显著高于健康对照组以及职业性尘肺病患者组(非结核性肺部疾病对照组)。(2)活动性肺结核患者中,双侧病灶肺结核患者组的血浆IL-6、IL-8水平显著高于单侧病灶肺结核患者组。(3)活动性肺结核患者中,菌阳性肺结核患者组血浆IL-6水平显著高于菌阴性肺结核患者组。(4)活动性肺结核患者中,γ-干扰素释放试验阴性患者组IFN-γ、IL-6水平显著高于健康对照组。(5)菌阴性肺结核患者中,γ-干扰素释放试验阴性患者组IFN-γ、IL-6水平显著高于健康对照组。结论IFN-γ、IL-6、IL-8可反映结核患者的炎症情况、疾病严重程度及细菌负荷,并且IFN-γ联合IL-6可以作为无病原学证据、免疫学检查结果为阴性且具有肺部影像学依据患者诊断的辅助指标,临床医师可以通过IFN-γ、IL-6的表达水平联合肺部影像学证据来为该类患者进行辅助诊断,并评估患者免疫状态,提高患者免疫力,为患者的个性化治疗提供依据。 展开更多
关键词 活动性肺结核 菌阴性肺结核 炎症细胞因子 ifn-Γ IL-6
下载PDF
Myricetin induces M2 macrophage polarization to alleviate renal tubulointerstitial fibrosis in diabetic nephropathy via PI3K/Akt pathway 被引量:3
15
作者 Wei-Long Xu Pei-Pei Zhou +6 位作者 Xu Yu Ting Tian Jin-Jing Bao Chang-Rong Ni Min Zha Xiao Wu Jiang-Yi Yu 《World Journal of Diabetes》 SCIE 2024年第1期105-125,共21页
BACKGROUND Development of end-stage renal disease is predominantly attributed to diabetic nephropathy(DN).Previous studies have indicated that myricetin possesses the potential to mitigate the pathological alterations... BACKGROUND Development of end-stage renal disease is predominantly attributed to diabetic nephropathy(DN).Previous studies have indicated that myricetin possesses the potential to mitigate the pathological alterations observed in renal tissue.Never-theless,the precise molecular mechanism through which myricetin influences the progression of DN remains uncertain.AIM To investigate the effects of myricetin on DN and explore its potential therapeutic mechanism.METHODS Db/db mice were administered myricetin intragastrically on a daily basis at doses of 50 mg/kg or 100 mg/kg for a duration of 12 wk.Subsequently,blood and urine indexes were assessed,along with examination of renal tissue pathology.Kidney morphology and fibrosis were evaluated using various staining techniques including hematoxylin and eosin,periodic acid–Schiff,Masson’s trichrome,and Sirius-red.Additionally,high-glucose culturing was conducted on the RAW 264.7 cell line,treated with 25 mM myricetin or co-administered with the PI3K/Akt inhibitor LY294002 for a period of 24 h.In both in vivo and in vitro settings,quantification of inflammation factor levels was conducted using western blotting,real-time qPCR and ELISA.RESULTS In db/db mice,administration of myricetin led to a mitigating effect on DN-induced renal dysfunction and fibrosis.Notably,we observed a significant reduction in expressions of the kidney injury markers kidney injury molecule-1 and neutrophil gelatinase associated lipocalin,along with a decrease in expressions of inflammatory cytokine-related factors.Furthermore,myricetin treatment effectively inhibited the up-regulation of tumor necrosis factor-alpha,interleukin-6,and interluekin-1βinduced by high glucose in RAW 264.7 cells.Additionally,myricetin modulated the M1-type polarization of the RAW 264.7 cells.Molecular docking and bioinformatic analyses revealed Akt as the target of myricetin.The protective effect of myricetin was nullified upon blocking the polarization of RAW 264.7 via inhibition of PI3K/Akt activation using LY294002.CONCLUSION This study demonstrated that myricetin effectively mitigates kidney injury in DN mice through the regulation of macrophage polarization via the PI3K/Akt signaling pathway. 展开更多
关键词 MYRICETIN Diabetic nephropathy PI3K/Akt pathway Renal tubulointerstitial fibrosis MACROPHAGE POLARIZATION
下载PDF
IFN-γ表达与食管癌患者细胞免疫水平及预后的相关性分析 被引量:1
16
作者 黄腾 黄维 +3 位作者 于大海 马珺 赵迪 鹿红 《现代肿瘤医学》 CAS 2024年第4期659-663,共5页
目的:探讨干扰素-γ(interferon gamma,IFN-γ)与食管癌患者细胞免疫水平及预后的相关性。方法:收集40例食管癌患者外周血标本,流式细胞仪检测标本中IFN-γ的浓度及CD4+T/CD8+T细胞比值;利用TISIDB数据库分析IFN-γ表达与免疫调控基因... 目的:探讨干扰素-γ(interferon gamma,IFN-γ)与食管癌患者细胞免疫水平及预后的相关性。方法:收集40例食管癌患者外周血标本,流式细胞仪检测标本中IFN-γ的浓度及CD4+T/CD8+T细胞比值;利用TISIDB数据库分析IFN-γ表达与免疫调控基因的关系;收集119例食管癌患者临床预后信息,利用Kaplan-Meier生存曲线分析IFN-γ表达与食管癌患者生存预后的相关性。结果:外周血中IFN-γ的浓度和CD4+T/CD8+T细胞比值呈负相关(R2=0.1662,P=0.009);食管癌组织中IFN-γ表达与免疫负调控基因CD274(rho=0.449,P<0.001)和PDCD1(rho=0.778,P<0.001)的表达呈正相关;IFN-γ高表达于食管癌组织(P<0.001),且IFN-γ高表达组患者的总生存(overall survival,OS)显著低于IFN-γ低表达组(P=0.008)。结论:IFN-γ在食管癌组织中的表达与细胞免疫水平呈负相关,同时可作为食管癌患者预后不良的指标。 展开更多
关键词 食管癌 ifn-Γ 细胞免疫 预后指标
下载PDF
二陈汤合三子养亲汤治疗慢性阻塞性肺疾病(痰湿蕴肺证)疗效及对肺功能、IFN-γ、ET-1的影响 被引量:3
17
作者 陈卜伟 周燕 +1 位作者 符海燕 蒙仕祥 《中华中医药学刊》 CAS 北大核心 2024年第1期230-233,共4页
目的探究二陈汤合三子养亲汤治疗慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)(痰湿蕴肺证)的疗效及对肺功能、伽马干扰素(interferon γ,IFN-γ)、内皮素(endothelin-1,ET-1)的影响。方法采用随机分组法将医院2019年... 目的探究二陈汤合三子养亲汤治疗慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)(痰湿蕴肺证)的疗效及对肺功能、伽马干扰素(interferon γ,IFN-γ)、内皮素(endothelin-1,ET-1)的影响。方法采用随机分组法将医院2019年2月—2022年3月收治的86例慢阻肺患者分为观察组与对照组,两组各43例。对照组采用西医常规治疗,观察组在此基础上联合使用二陈汤合三子养亲汤治疗。观察两组患者治疗前后肺功能、蛋白质羰基(protein carbonyl content,PC)、8-羟基脱氧鸟苷(8-hydroxy-2 deoxyguanosine,8-OHdG)、丙二醛(malonic aldehyde,MDA)含量和IFN-γ、ET-1。观察两组患者临床症状消失时间和临床疗效。结果两组患者治疗后FEV1、PEF和Ppeak水平显著高于治疗前(P<0.05)。治疗后,观察组FEV1、PEF和Ppeak水平显著高于对照组(P<0.05)。两组患者治疗后PC、8-OHdG和MDA水平显著低于治疗前(P<0.05)。治疗后,观察组PC、8-OHdG和MDA水平显著低于对照组(P<0.05)。两组患者治疗后IFN-γ和ET-1水平显著低于治疗前(P<0.05)。治疗后,观察组IFN-γ和ET-1水平显著低于对照组(P<0.05)。观察组临床症状消失时间显著快于对照组(P<0.05)。观察组总有效率为83.72%(36/43)显著高于对照组(65.12%,28/43)(χ^(2)=3.909,P=0.048)。结论二陈汤合三子养亲汤能有效改善慢阻肺患者肺功能,降低氧化应激相关产物蛋白质的含量,减少临床症状持续时间,利于降低FN-γ、ET-1水平,临床疗效得到显著提升。 展开更多
关键词 二陈汤 三子养亲汤 慢阻肺 痰湿蕴肺证 肺功能 ifn-Γ ET-1
下载PDF
Cyanidin-3-glucoside protects the photooxidative damage of retinal pigment epithelium cells by regulating sphingolipid signaling and inhibiting MAPK pathway 被引量:1
18
作者 Tingting Liu Wentao Qi +2 位作者 Wenting Peng Jianan Zhang Yong Wang 《Food Science and Human Wellness》 SCIE CSCD 2024年第2期621-632,共12页
Cyanidin-3-glucoside(C3G)is the most common anthocyanin in dark grains and berries and is a food functional factor to improve visual health.However,the mechanisms of C3G on blue light-induced retinal pigment epithelia... Cyanidin-3-glucoside(C3G)is the most common anthocyanin in dark grains and berries and is a food functional factor to improve visual health.However,the mechanisms of C3G on blue light-induced retinal pigment epithelial(RPE)cell photooxidative damage needs further exploration.We investigated the effects of C3G on blue light-irradiated A2E-containing RPE cells and explored whether sphingolipid,mitogen-activated protein kinase(MAPK),and mitochondria-mediated pathways are involved in this mechanism.Blue light irradiation led to mitochondria and lysosome damage in RPE cells,whereas C3G preserved mitochondrial morphology and function and maintained the lysosomal integrity.C3G suppressed the phosphorylation of JNK and p38 MAPK and mitochondria-mediated pathways to inhibit RPE cell apoptosis.Lipidomics data showed that C3G protected RPE cells against blue light-induced lipid peroxidation and apoptosis by maintaining sphingolipids balance.C3G significantly inhibited ceramide(Cer d18:0/15:0,Cer d18:0/16:0 and Cer d18:0/18:0)accumulation and elevated galactosylceramide(GalCer d18:1/15:0 and GalCer d18:1/16:0)levels in the irradiated A2E-containing RPE cells.Furthermore,C3G attenuated cell membrane damage by increasing phosphatidylcholine and phosphatidylserine levels.C3G inhibited apoptosis and preserved the structure of mitochondria and lysosome by regulating sphingolipid signaling and suppression of MAPK activation in RPE cells.Thus,dietary supplementation of C3G prevents retinal photooxidative damage. 展开更多
关键词 Cyanidin-3-glucoside CERAMIDE MAPK pathway Mitochondria-dependent apoptosis Lipidomics analysis
下载PDF
Silencing of peroxiredoxin 2 suppresses proliferation and Wnt/β-catenin pathway,and induces senescence in hepatocellular carcinoma 被引量:1
19
作者 XUEGANG YANG XIANHONG XIANG +3 位作者 GUOHUI XU SHI ZHOU TIANZHI AN ZHI HUANG 《Oncology Research》 SCIE 2024年第1期213-226,共14页
Hepatocellular carcinoma(HCC),a common malignancy worldwide,still lacks effective clinical treatment.The study aimed to investigate the oncogenes that affect the progression of HCC and their possible mechanisms.In our... Hepatocellular carcinoma(HCC),a common malignancy worldwide,still lacks effective clinical treatment.The study aimed to investigate the oncogenes that affect the progression of HCC and their possible mechanisms.In our study,we initially confirmed a higher level of PRDX2 in the bile of HCC patients compared to those with choledocholithiasis by 2-DE,LC-MS,and ELISA.Subsequently,we demonstrated the high expression of peroxiredoxin 2(PRDX2)in HCC based on the TCGA database and clinical sample analysis.Furthermore,PRDX2 overexpression enhanced the viability of HCC cells.And PRDX2 silencing induced senescence of HCC cells.In vivo,knockdown of PRDX2 significantly reduced the weight of xenograft tumors.PRDX2 also was found to activate the Wnt/β-catenin pathway by inducingβ-catenin nuclear translocation.Consequently,we proved that silencing PRDX2 could inhibit proliferation and Wnt/β-catenin pathway while promoting senescence in HCC cells. 展开更多
关键词 Peroxiredoxin 2 Hepatocellular carcinoma Wnt/β-catenin pathway SENESCENCE PROLIFERATION
下载PDF
Activation of the wnt/β-catenin/CYP1B1 pathway alleviates oxidative stress and protects the blood-brain barrier under cerebral ischemia/reperfusion conditions 被引量:7
20
作者 Xingyong Chen Nannan Yao +4 位作者 Yanguang Mao Dongyun Xiao Yiyi Huang Xu Zhang Yinzhou Wang 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第7期1541-1547,共7页
Accumulating evidence suggests that oxidative stress and the Wnt/β-catenin pathway participate in stroke-induced disruption of the blood-brain barrier.However,the potential links between them following ischemic strok... Accumulating evidence suggests that oxidative stress and the Wnt/β-catenin pathway participate in stroke-induced disruption of the blood-brain barrier.However,the potential links between them following ischemic stroke remain largely unknown.The present study found that cerebral ischemia leads to oxidative stress and repression of the Wnt/β-catenin pathway.Meanwhile,Wnt/β-catenin pathway activation by the pharmacological inhibito r,TWS119,relieved oxidative stress,increased the levels of cytochrome P4501B1(CYP1B1)and tight junction-associated proteins(zonula occludens-1[ZO-1],occludin and claudin-5),as well as brain microvascular density in cerebral ischemia rats.Moreove r,rat brain microvascular endothelial cells that underwent oxygen glucose deprivation/reoxygenation displayed intense oxidative stress,suppression of the Wnt/β-catenin pathway,aggravated cell apoptosis,downregulated CYP1B1and tight junction protein levels,and inhibited cell prolife ration and migration.Overexpression ofβ-catenin or knockdown ofβ-catenin and CYP1B1 genes in rat brain mic rovascular endothelial cells at least partly ameliorated or exacerbated these effects,respectively.In addition,small interfering RNA-mediatedβ-catenin silencing decreased CYP1B1 expression,whereas CYP1B1 knoc kdown did not change the levels of glycogen synthase kinase 3β,Wnt-3a,andβ-catenin proteins in rat brain microvascular endothelial cells after oxygen glucose deprivatio n/reoxygenation.Thus,the data suggest that CYP1B1 can be regulated by Wnt/β-catenin signaling,and activation of the Wnt/β-catenin/CYP1B1 pathway contributes to alleviation of oxidative stress,increased tight junction levels,and protection of the blood-brain barrier against ischemia/hypoxia-induced injury. 展开更多
关键词 blood-brain barrier CYP1B1 oxidative stress oxygen glucose deprivation/reoxygenation tight junction vascular endothelial cells Wnt/β-catenin pathway β-catenin
下载PDF
上一页 1 2 250 下一页 到第
使用帮助 返回顶部