机译:Porphyromonas Gingivalis Porphyromonas Gingivalis的脂多糖通过激活NF-κB和JNK信号传导途径引起过度的肝脂肪累积
School of StomatologyWeifang Medical UniversityWeifang China;
Shanghai Engineering Research Center of Tooth Restoration and Regeneration Department of;
CAS Key Laboratory of Nutrition Metabolism and Food Safety Shanghai Institute of Nutrition and;
Shanghai Engineering Research Center of Tooth Restoration and Regeneration Department of;
CAS Key Laboratory of Nutrition Metabolism and Food Safety Shanghai Institute of Nutrition and;
CAS Key Laboratory of Nutrition Metabolism and Food Safety Shanghai Institute of Nutrition and;
Shanghai Engineering Research Center of Tooth Restoration and Regeneration Department of;
JNK; NF‐κB; non‐alcoholic fatty liver disease; periodontitis; Porphyromonas gingivalis;
机译:Porphyromonas Gingivalis Porphyromonas Gingivalis的脂多糖通过激活NF-κB和JNK信号传导途径引起过度的肝脂肪累积
机译:核因子-βB和p38丝裂原激活的蛋白激酶信号转导通路与牙龈卟啉单胞菌脂多糖诱导人口腔角质形成细胞脂多糖结合蛋白表达至关重要
机译:蜂毒通过抑制NF-κB和AP-1信号通路抑制牙龈卟啉单胞菌脂多糖诱导的促炎性细胞因子
机译:映射涉及暴露于卟啉核糖菌的THP-1细胞中涉及的刺激特异性信令途径VS FIMBRIA VS Live P.G。
机译:口腔粘膜脂质对牙龈卟啉单胞菌具有抗菌作用,可诱导超微结构损伤,并改变细菌脂质和蛋白质组成
机译:蜂毒通过抑制NF-κB和AP-1信号通路抑制牙龈卟啉单胞菌脂多糖诱导的促炎性细胞因子
机译:通过差异激活TLR2 / 4介导的NF-κB/ stat3信号传导途径,吡喃替莫氏菌宫内节花的制剂诱导BV-2微胶质细胞中的免疫炎症反应比大肠杆菌在大肠杆菌中产生较弱的免疫炎症反应