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机译:Gamma-mangostin通过HepG2和L02细胞的SIRT1 / LKB1 / AMPK途径改善游离脂肪酸诱导的脂质积累
Shenzhen Univ Shenzhen Key Lab Marine Bioresource &
Ecoenvironm Guangdong Prov Key Lab Plant Epigenet Coll Life S Coll Optoelect Engn Minist Educ &
Guangdong Prov Shenzhen 518060 Guangdong Peoples R China;
Shenzhen Univ Shenzhen Key Lab Marine Bioresource &
Ecoenvironm Guangdong Prov Key Lab Plant Epigenet Coll Life S Coll Optoelect Engn Minist Educ &
Guangdong Prov Shenzhen 518060 Guangdong Peoples R China;
Shenzhen Univ Gen Hosp Dept Dermatol Shenzhen 518055 Guangdong Peoples R China;
Shenzhen Univ Shenzhen Key Lab Marine Bioresource &
Ecoenvironm Guangdong Prov Key Lab Plant Epigenet Coll Life S Coll Optoelect Engn Minist Educ &
Guangdong Prov Shenzhen 518060 Guangdong Peoples R China;
Shenzhen Univ Gen Hosp Dept Spine Surg Shenzhen 518055 Guangdong Peoples R China;
Shenzhen Univ Shenzhen Key Lab Marine Bioresource &
Ecoenvironm Guangdong Prov Key Lab Plant Epigenet Coll Life S Coll Optoelect Engn Minist Educ &
Guangdong Prov Shenzhen 518060 Guangdong Peoples R China;
Shenzhen Univ Shenzhen Key Lab Marine Bioresource &
Ecoenvironm Guangdong Prov Key Lab Plant Epigenet Coll Life S Coll Optoelect Engn Minist Educ &
Guangdong Prov Shenzhen 518060 Guangdong Peoples R China;
Shenzhen Univ Shenzhen Key Lab Marine Bioresource &
Ecoenvironm Guangdong Prov Key Lab Plant Epigenet Coll Life S Coll Optoelect Engn Minist Educ &
Guangdong Prov Shenzhen 518060 Guangdong Peoples R China;
Shenzhen Univ Shenzhen Key Lab Marine Bioresource &
Ecoenvironm Guangdong Prov Key Lab Plant Epigenet Coll Life S Coll Optoelect Engn Minist Educ &
Guangdong Prov Shenzhen 518060 Guangdong Peoples R China;
the AMPK pathway; Compound C; alpha-mangostin; gamma-mangostin; nonalcoholic fatty liver disease (NAFLD);
机译:Gamma-mangostin通过HepG2和L02细胞的SIRT1 / LKB1 / AMPK途径改善游离脂肪酸诱导的脂质积累
机译:Coniferaldehyde通过LKB1 / AMPK信号通路改善棕榈酸诱导的HEPG2细胞中的脂质和葡萄糖代谢
机译:Zanthoxylum的异常通过HepG2细胞中的LKB1 / AMPK途径抑制油酸诱导的脂质积累
机译:培养细胞中的多不饱和脂肪酸,脂质蓄积和氧化剂胁迫。
机译:更正为花椒通过激活HepG2细胞中的LKB1 / AMPK途径抑制油酸诱导的脂质蓄积
机译:Zanthoxylum的异常通过HepG2细胞中的LKB1 / AMPK途径抑制油酸诱导的脂质积累