机译:通过α-高压运动激活肝脏Inkt2细胞改善C57BL / 6J小鼠高脂饮食诱导的肝脏脂肪变性
Key Lab Pathogenesis Mech &
Control Inflammatory Baoding Peoples R China;
Key Lab Pathogenesis Mech &
Control Inflammatory Baoding Peoples R China;
Hebei Univ Affiliated Hosp Baoding 071000 Hebei Peoples R China;
Key Lab Pathogenesis Mech &
Control Inflammatory Baoding Peoples R China;
Key Lab Pathogenesis Mech &
Control Inflammatory Baoding Peoples R China;
Key Lab Pathogenesis Mech &
Control Inflammatory Baoding Peoples R China;
Key Lab Pathogenesis Mech &
Control Inflammatory Baoding Peoples R China;
Key Lab Pathogenesis Mech &
Control Inflammatory Baoding Peoples R China;
Nonalcoholic fatty liver disease (NAFLD); iNKT1/iNKT2; alpha-Galactosylceramide (alpha-GalCer); Cytokine; Transcription factor;
机译:通过α-高压运动激活肝脏Inkt2细胞改善C57BL / 6J小鼠高脂饮食诱导的肝脏脂肪变性
机译:Myricetin通过在C57BL / 6J小鼠中作用于MicroRNA-146B /甲状腺激素受体B途径来缓解肝脏脂肪变性
机译:GLP-1模拟,Liraglutide,改善C57BL / 6J小鼠中的肝脏脂肪变性和心脏肥厚
机译:DMDMDX / J和C57BL / 6J小鼠全血参考值的比较使用中子激活分析
机译:脂蛋白受体SR-B1缺乏增强脂肪组织炎症,并在小鼠饮食诱导的肥胖期间减少对肝脏脂肪变性的易感性
机译:Glp-1类似物利拉鲁肽可改善以西方饮食喂养的C57BL / 6J小鼠的肝脏脂肪变性和心脏肥大
机译:GinkGolide B降低体重并改善高脂饮食诱导的肥胖小鼠的肝脏脂肪变性与妊娠X受体活化相关