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Apigenin ameliorates diabetic neuropathy in rats by modulating the TLR4/MyD88 signaling pathway

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Asian Pacific Journal of Tropical Biomedicine 2023年第11期13卷 469-478,I0003,I0004,I0005,I0006,I0008页

作者： Yan-Bo Yu Mi-Zhen Qiu Da-Ying Zhang Department of Pain The First Affiliated Hospital of Nanchang UniversityNanchang 330006China

Objective:To determine the neuroprotective effects of apigenin against streptozotocin(STZ)-induced diabetic neuropathy(DN).Methods:To induce DN,Wistar rats(150-200 g)were administered with STZ(55 mg/kg,i.p.).Then they were randomly assigned to various groups,viz.,normal,diabetic control,insulin(10 IU/kg,s.c.),apigenin(5,10,and 20 mg/kg,p.o.),and insulin(10 IU/kg)plus apigenin(20 mg/kg,p.o.).Various behavioral,biochemical,and molecular markers[tumor necrosis factor-alpha(TNF-α),interleukin(IL)-1β,IL-6,Toll-like receptor 4(TLR4),myeloid differentiation primary response 88(MyD88),and nuclear factor erythroid 2-related factor 2(Nrf2)]were assessed.Results:Apigenin(10 and 20 mg/kg,p.o.)substantially reduced plasma glucose levels,lipid profile,aspartate transaminase,alanine transaminase,glycated hemoglobin,and neural advanced glycation end products in STZ-induced DN rats(PMyD88(PMyD88 signaling pathway.

关键词： Apigenin Diabetic neuropathy MyD88 Nrf2 Proinflammatory cytokines TLR4

HSA-MIR-203/MyD88 axis mediates the protective effect of hispidulin on LPS-induced apoptosis in a human renal tubular epithelial line,HK-2

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BIOCELL 2022年第1期46卷 149-158页

作者： SICONG WANG RUIJIN LIU QIUYUAN HAN KAIJIANG YU Department of Critical Care Medicine The Second Affiliated Hospital of Harbin Medical UniversityHarbin150001China Department of Critical Care Medicine The Cancer Hospital of Harbin Medical UniversityHarbin150081China Department of Critical Care Medicine The First Affiliated Hospital of Harbin Medical UniversityHarbin150001China

Acute kidney injury(AKI),commonly occurring as complications of sepsis,cardiac surgery,and liver or kidney transplantation,is a critical care syndrome.It is well known that lipopolysaccharide(LPS)shock is a common triggering factor for AKI.This study is aimed to examine the effect of flavonoid compound hispidulin on LPS-induced AKI.For this,renal tubular epithelial cell HK-2 was treated with LPS to establish an in vitro model of AKI.The effect of hispidulin on HK-2 cell viability was examined using CCK-8 assay.Cell apoptosis was determined by TUNEL and flow cytometry.Apoptosis marker proteins were determined by using western blot.The levels of pro-inflammatory cytokines were determined by ELISA assay and qRT-PCR.The translocation of NF-κB was determined by western blot.The effect of MyD88 on the cytoprotective activities of hispidulin was examined by overexpressing MyD88 in HK-2 cells.Our results showed that hispidulin was not able to produce a cytotoxic effect on HK-2 cells at tested concentrations.However,hispidulin could protect HK-2 cells from LPS-induced cell injury.Our results also showed that hispidulin was able to attenuate LPS-induced HK-2 cell apoptosis.In addition,LPS led to an inflammatory response in HK-2 cells,evidenced by NF-κB p65 activation as well as increased expression and release of inflammatory cytokine IL-6 and TNF-α,which could be reversed by pretreatment with hispidulin.Overexpression MyD88 was found to significantly dampen the cytoprotective activities of hispidulin against LPS insult.More importantly,MyD88 was identified as a direct target of hsa-miR-203,and hispidulin was found to regulate the expression of MyD88 via upregulating hsa-miR-203.Our results showed that hispidulin attenuates LPS-induced HK-2 damage via regulating hsa-miR-203/MyD88 axis.

关键词： Hispidulin LPS HK-2 hsa-miR-203 MyD88

Cardamine komarovii flower extract reduces lipopolysaccharide-induced acute lung injury by inhibiting MyD88/TRIF signaling pathways

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Chinese Journal of Natural Medicines 2019年第6期17卷 461-468页

作者： CHEN Qi ZHANG Ke-Xin LI Tai-Yuan PIAO Xuan-Mei LIAN Mei-Lan AN Ren-Bo JIANG Jun Key Laboratory of Natural Resource of Changbai Mountain and Functional Molecules(Ministry of Education) Yanbian UniversityYanji 133002China Agricultural College Yanbian UniversityYanji 133002China Department of Urology College of MedicineChungbuk National UniversityCheongju 28644Republic of Korea

In the present study, we investigated anti-inflammatory effect of Cardamine komarovii flower(CKF) on lipopolysaccharide(LPS)-induced acute lung injury(ALI). We determined the effect of CKF methanolic extracts on LPS-induced pro-inflammatory mediators NO and prostaglandin E2(PGE2), production of pro-inflammatory cytokines(IL-1β, TNF-α, and IL-6), and related protein expression levels of MyD88/TRIF signaling pathways in peritoneal macrophages(PMs). Nuclear translocation of NF-κB-p65 was analyzed by immunofluorescence. For the in vivo experiments, an ALI model was established to detect the number of inflammatory cells and inflammatory factors(IL-1β, TNF-α, and IL-6) in bronchoalveolar lavage fluid(BALF) of mice. The pathological damage in lung tissues was evaluated through H&E staining. Our results showed that CKF can decrease the production of inflammatory mediators, such as NO and PGE2, by inhibiting their synthesis-related enzymes i NOS and COX-2 in LPS-induced PMs. In addition, CKF can downregulate the mRNA levels of IL-1β, TNF-α, and IL-6 to inhibit the production of inflammatory factors. Mechanism studies indicated that CKF possesses a fine anti-inflammatory effect by regulating My D88/TRIF dependent signaling pathways. Immunocytochemistry staining showed that the CKF extract attenuates the LPS-induced translocation of NF-kB p65 subunit in the nucleus from the cytoplasm. In vivo experiments revealed that the number of inflammatory cells and IL-1β in BALF of mice decrease after CKF treatment. Histopathological observation of lung tissues showed that CKF can remarkably improve alveolar clearance and infiltration of interstitial and alveolar cells after LPS stimulation. In conclusion, our results suggest that CKF inhibits LPS-induced inflammatory response by inhibiting the MyD88/TRIF signaling pathways, thereby protecting mice from LPS-induced ALI.

关键词： Cardamine komarovii flower Inflammation MyD88 TRIF Acute lung injury

TLR4/MyD88信号通路在膝骨关节炎滑膜炎中的作用

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中国骨质疏松杂志 2022年第11期28卷 1690-1694页

作者：韩宪富李宁谢兴文黄委委李辉甘肃中医药大学中医临床学院甘肃兰州730000 甘肃中医药大学附属医院康复骨科甘肃兰州730020 甘肃中医药大学附属医院老年骨科甘肃兰州730030

Toll样受体4是重要的固有免疫模式识别受体,通过识别损伤相关分子模式及病原相关分子模式,启动髓样分化因子88依赖途径后激活NF-κB信号通路,引发炎性介质及细胞因子的分泌,触发固有免疫应答,在膝骨关节炎滑膜炎的发生中发挥作用。研究T... 详细信息

Toll样受体4是重要的固有免疫模式识别受体,通过识别损伤相关分子模式及病原相关分子模式,启动髓样分化因子88依赖途径后激活NF-κB信号通路,引发炎性介质及细胞因子的分泌,触发固有免疫应答,在膝骨关节炎滑膜炎的发生中发挥作用。研究TLR4/MyD88信号通路在膝骨关节炎滑膜炎中的作用,以期更深入的阐明膝骨关节炎滑膜炎发病机制,为膝骨关节炎滑膜炎的诊疗提供理论依据和参考。

关键词： TLR4 MyD88 膝骨关节炎滑膜炎

RAW264.7细胞MyD88基因缺失株构建

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中国免疫学杂志 2022年第14期38卷 1739-1743页

作者：王燕陈为董明鑫孙成彪张剑旭常影刘文森许娜中国农业科学院长春兽医研究所长春130122 吉林医药学院吉林132013

目的:构建MyD88基因缺失的RAW264.7细胞株,为探寻MyD88基因的作用提供重要载体。方法:制备HBLV-Cas9-PURO慢病毒,感染RAW264.7细胞,得到RAW264.7-Cas9细胞株。依据CRISPR/Cas9系统原理,设计3条靶向MyD88基因的sgRNA,慢病毒包装后感染RAW264.7-Cas9细胞株,观察感染效果,PCR和Western blot验证MyD88基因敲除水平并筛选稳转细胞株。选取敲除效果最佳株,经LPS和PGN诱导后,荧光定量PCR和ELISA检测TNF-α表达和分泌。结果:HBLV-Cas9-PURO感染后RAW264.7细胞Cas9基因扩增明显升高,RAW264.7-Cas9细胞株构建成功。包装目的基因的慢病毒感染RAW264.7-Cas9后,荧光显微镜观察导入成功;PCR显示与对照组相比,HBLV-m-MyD88 gRNA3-GFP感染后MyD88基因表达显著下调;Western blot进一步证实,HBLV-m-MyD88 gRNA1-GFP和HBLV-m-MyD88 gRNA3-GFP感染后MyD88蛋白表达下降,且HBLV-m-MyD88 gRNA3-GFP组下降最为显著。LPS和PGN诱导HBLV-m-MyD88 gRNA3-GFP组细胞后,TNF-α表达和分泌水平均下调。结论:利用慢病毒介导的CRISPR/Cas9技术成功构建稳定敲除MyD88基因的RAW264.7细胞株。

关键词：慢病毒 CRISPR/Cas9 MyD88 RAW264.7细胞

硒缺乏通过TLR4/MyD88/NF-κB信号通路介导鸡胸腺细胞凋亡

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畜牧兽医学报 2022年第11期53卷 4035-4047页

作者：张瑞莉张迪郭荣陈阳李广兴黄小丹东北农业大学动物医学院哈尔滨150030 黑龙江省实验动物与比较医学重点实验室哈尔滨150030

本试验旨在探讨硒缺乏是否通过激活Toll样受体信号通路诱导鸡胸腺细胞凋亡。复制硒缺乏模型,将200只1日龄健康的肉鸡随机分为对照组(C组)和缺硒组(L组),对照组饲喂硒含量0.2 mg·kg^(-1)的正常日粮,缺硒组饲喂硒含量0.004 mg·kg^(-1)... 详细信息

本试验旨在探讨硒缺乏是否通过激活Toll样受体信号通路诱导鸡胸腺细胞凋亡。复制硒缺乏模型,将200只1日龄健康的肉鸡随机分为对照组(C组)和缺硒组(L组),对照组饲喂硒含量0.2 mg·kg^(-1)的正常日粮,缺硒组饲喂硒含量0.004 mg·kg^(-1)的缺硒日粮。在15、25、35、45、55日龄时,每组分别选取15只鸡,观察胸腺组织病理形态变化和超微结构变化;检测胸腺组织中TLR4信号转导通路与细胞凋亡相关因子的表达。又建立了MDCC-MSB1(MSB1)细胞硒缺乏模型,并在此基础上设立6个分组:对照(C group)组、缺硒(L group)组、缺硒+转染空质粒(L+pCMV-HA-N)组、缺硒+siRNA阴性对照(L+NCsiRNA)组和缺硒+过表达TLR4(L+pCMV-HA-TLR4)组、缺硒+干扰TLR4(L+siChTLR4)组,低硒处理5 d后,检测细胞活力、细胞凋亡情况、TLR4信号转导通路与细胞凋亡相关因子的表达。结果显示:1)与C组相比,L组皮质髓质的淋巴细胞数量减少、细胞排列紊乱、皮质髓质充血、核碎裂,广泛的局灶性坏死。L组鸡胸腺组织淋巴细胞间出现裂隙,体积缩小,细胞碎裂,核染色质边集,线粒体肿胀,嵴断裂。2)与15日龄C组相比,L组鸡胸腺中TLR4、MyD88、NF-κB、Caspase-3、Caspase-9、Bax mRNA和蛋白表达水平在15~55日龄中均显著上调,Bcl-2 mRNA和蛋白表达水平呈相反趋势。3)与C组相比,L组MSB1细胞活力显著下降、细胞凋亡数量明显增加、TLR4、MyD88、NF-κB、Caspase-3、Caspase-9、Bax mRNA和蛋白的表达均显著增加、Bcl-2 mRNA和蛋白表达水平极显著降低;与L组相比,L+siChTLR4组细胞活力明显增强、细胞凋亡数量明显减少、相关因子mRNA和蛋白表达显著下降,而L+pCMV-HA-TLR4组细胞活力明显降低、细胞凋亡数量明显增加、相关因子mRNA和蛋白表达均明显增加。综上所述,硒缺乏通过TLR4/MyD88/NF-κB信号通路介导鸡胸腺细胞凋亡,并进一步诱导鸡胸腺损伤。

关键词：硒缺乏 TLR4 MyD88 NF-κB 胸腺凋亡

弥漫大B细胞淋巴瘤中MyD88、CD79B基因特征与临床病理及预后的关系

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临床与实验病理学杂志 2022年第9期38卷 1072-1077页

作者：吴灿张大川王辉雷婷史勇强谢雯莹贾晨昊李青苏州大学附属第三医院病理科常州213003

目的探讨弥漫大B细胞淋巴瘤(diffuse large B-cell lymphoma,DLBCL)中MyD88、CD79B基因突变与其临床病理特征及预后的相关性。方法对2016年10月~2020年7月苏州大学附属第三医院89例经病理学诊断的DLBCL进行回顾性分析。应用二代测序技... 详细信息

目的探讨弥漫大B细胞淋巴瘤(diffuse large B-cell lymphoma,DLBCL)中MyD88、CD79B基因突变与其临床病理特征及预后的相关性。方法对2016年10月~2020年7月苏州大学附属第三医院89例经病理学诊断的DLBCL进行回顾性分析。应用二代测序技术检测患者基因变异情况,并分析MyD88、CD79B基因与临床病理特征及预后的关系。结果89例DLBCL中MyD88基因突变、CD79B基因突变和MyD88/CD79B基因双突变的频率分别为20.2%、21.3%、6.7%。MyD88基因在非生发中心B细胞(non-germinal center B-cell-like,non-GCB)型、BCL-2阳性、c-MYC/BCL-2双阳性和Ki-67增殖指数高的病例中具有较高的突变频率(PMyD88/CD79B基因双突变在c-MYC/BCL-2双阳性及Ki-67增殖指数高的病例中具有较高的突变频率(PMyD88基因突变和MyD88/CD79B基因双突变病例在中期疗效评估时其完全缓解率均低于非突变病例(PMyD88基因突变和MyD88/CD79B基因双突变患者的总生存期及无进展生存期均低于非突变组(PMyD88基因突变DLBCL更常见于non-GCB型,具有较高的Ki-67增殖指数、BCL-2阳性和c-MYC/BCL-2共阳性的特点;CD79B基因突变DLBCL更常见于non-GCB型,Ki-67增殖指数较高;MyD88/CD79B基因双突变DLBCL具有较高的Ki-67增殖指数和c-MYC/BCL-2共阳性的特点。MyD88基因突变、MyD88/CD79B基因双突变影响DLBCL患者化疗效果及长期生存。

关键词：弥漫大B细胞淋巴瘤 MyD88 CD79B 治疗效果

MyD88抑制剂对小鼠炎症相关肝细胞癌的抑制作用及机制研究

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MyD88抑制剂对小鼠炎症相关肝细胞癌的抑制作用及机制研究

作者：尚润石华中科技大学

学位级别：硕士

目的:探究自创的MyD88抑制剂TJ-M2010-5(TJ-5)在二乙基亚硝胺诱导的小鼠肝细胞癌发生发展中的作用及机制。方法:1.体内实验:选取出生后第15日龄的雄性C57BL/6小鼠,单次腹腔注射30mg/kg二乙基亚硝胺(diethylnitrosamine,DEN)建立小鼠肝... 详细信息

目的:探究自创的MyD88抑制剂TJ-M2010-5(TJ-5)在二乙基亚硝胺诱导的小鼠肝细胞癌发生发展中的作用及机制。方法:1.体内实验:选取出生后第15日龄的雄性C57BL/6小鼠,单次腹腔注射30mg/kg二乙基亚硝胺(diethylnitrosamine,DEN)建立小鼠肝细胞癌模型。小鼠分为3组:正常对照组(Control组):腹腔注射生理盐水;模型组(DEN组):腹腔注射30mg/kg DEN;MyD88抑制剂组(TJ-5组):在第一次DEN给药前2天开始,每天腹腔注射50mg/kg TJ-5,直至观察期结束。三组小鼠持续观察40周,通过肝脏肿瘤个数、最大肿瘤直径、肝体重比、血清转氨酶水平以及H&E染色评估肝脏肿瘤进展。WB检测造模后各组小鼠肝脏STAT3和YAP蛋白的核浆迁移情况。选取8周的雄性C57BL/6小鼠,单次腹腔注射100mg/kg DEN建立小鼠急性期肝损伤模型,实验分组同上。DEN注射48h后H&E染色、血清转氨酶检测评估肝脏损伤程度,ELISA和q RT-PCR检测血清和肝脏中IL-6的表达水平。WB检测肝脏TLR4、MyD88蛋白的表达水平以及STAT3蛋白的磷酸化水平。2.体外实验:分离获取8周龄雄性C57BL/6小鼠骨髓细胞,体外培养成骨髓来源的巨噬细胞(Bone marrow derived macrophage,BMDM)并予以30μmol/L TJ-5处理2h后,再用小鼠原代肝细胞冻融裂解制备的条件培养液刺激24h,流式细胞术检测F4/80MHC II、F4/80CD80以及F4/80CD86细胞比例,q RT-PCR和ELISA检测BMDM中IL-6的生成。小鼠肝癌细胞系Hepa1-6予以50ng/ml IL-6刺激2h后,q RT-PCR检测YAP蛋白下游靶基因CTGF、CYR61转录情况,免疫荧光和WB检测YAP蛋白核浆迁移情况,免疫共沉淀检测STAT3和YAP的相互作用。结果:1.体内实验:成功建立小鼠肝细胞癌模型:DEN注射40周后,模型组小鼠肿瘤明显形成,MyD88抑制剂组小鼠肿瘤数目、最大肿瘤直径以及肝体重比明显较DEN组降低。WB结果显示与DEN组相比,TJ-5干预显著抑制了YAP和STAT3蛋白的核易位。急性期肝损伤模型:H&E染色显示DEN组小鼠肝脏小叶中心区出现了广泛的肝细胞变性坏死,而TJ-5干预明显减轻了肝细胞的损伤。血清学检测显示与DEN组相比,TJ-5显著降低了血清ALT、AST以及IL-6的水平。WB结果显示TJ-5明显降低肝脏TLR4/MyD88蛋白的表达并抑制STAT3蛋白的磷酸化。2.体外实验:小鼠原代肝细胞冻融裂解制备的条件培养液刺激小鼠BMDM后,流式细胞术结果显示F4/80MHC II、F4/80CD80以及F4/80CD86细胞比例明显升高;而TJ-5干预可降低上述细胞比例。ELISA和q RT-PCR结果显示TJ-5干预可明显抑制BMDM IL-6的产生。WB和免疫荧光结果显示小鼠肝癌细胞系Hepa1-6在IL-6刺激下YAP核易位水平明显增加,免疫共沉淀结果显示IL-6促进STAT3和YAP的相互作用,si RNA敲低STAT3后YAP核易位水平明显降低。结论:1.MyD88参与了DEN诱导的小鼠肝细胞癌的进展;2.MyD88抑制剂TJ-5能够抑制肝细胞冻融裂解液诱导的巨噬细胞活化以及炎性细胞因子IL-6的分泌;3.TJ-5通过减少STAT3和YAP的结合抑制YAP核易位,进而抑制肝脏肿瘤的进展。

关键词：肝细胞癌巨噬细胞 MyD88 IL-6 STAT3 YAP

鸡MyD88基因对巨噬细胞增殖和凋亡的影响

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中国兽医学报 2023年第8期43卷 1703-1709页

作者：丁梦霞朱召岩于燕鸽王冰欣昝瑞隆田亚东孙桂荣韩瑞丽蒋瑞瑞康相涛闫峰宾河南农业大学动物医学院河南郑州450046 河南农业大学动物科技学院河南郑州450046

为探究鸡MyD88基因对巨噬细胞增殖和凋亡的影响,通过构建MyD88基因过表达质粒,以及合成MyD88基因干扰片段,并分别转染至鸡巨噬细胞(HD11)细胞中,采用CCK-8、流式细胞术及qRT-PCR方法检测过表达和干扰MyD88对HD11细胞增殖和凋亡的影响。... 详细信息

为探究鸡MyD88基因对巨噬细胞增殖和凋亡的影响,通过构建MyD88基因过表达质粒,以及合成MyD88基因干扰片段,并分别转染至鸡巨噬细胞(HD11)细胞中,采用CCK-8、流式细胞术及qRT-PCR方法检测过表达和干扰MyD88对HD11细胞增殖和凋亡的影响。结果显示,MyD88过表达可显著降低HD11细胞活力(PMyD88可显著提高HD11细胞活力(PMyD88基因能抑制HD11细胞增殖,促进HD11细胞凋亡。

关键词：鸡 MyD88 HD11细胞增殖凋亡