Yan Yan, Liu Chunyan, Zhao Shimin, Wang Xinxu, Wang Jinling, Zhang Heping, Wang Yuzhen, Zhao Guofen
College of Life Science, Inner Mongolia Agricultural University, Hohhot, 010018, People's Republic of China.
College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot, 010018, People's Republic of China.
AMB Express. 2020 May 29;10(1):101. doi: 10.1186/s13568-020-01038-y.
Both steatosis and inflammation are key pathological events in the progression of non-alcoholic fatty liver disease (NAFLD). Probiotics are beneficial for the prevention and treatment of NAFLD. Bifidobacterium animalis subsp. lactis V9 (V9) is a newly isolated strain with favorable probiotic properties. The study aims to evaluate the effects and mechanisms of V9 on the hepatic steatosis and inflammatory responses in a rat model of NAFLD induced by high-fat diets (HFD). Our results showed that administration of V9 significantly attenuated the HFD-induced increases in alanine transaminase (ALT) and aspartate aminotransferase (AST) levels, resulting in alleviated hepatic steatosis. V9 supplementation reduced the accumulation of hepatic triglyceride and free fatty acid,while increasing the levels of glycogen. Serum levels of glucose were also decreased in HFD rats administrated with V9. Meanwhile, the transcription of SREBP-1c and FAS was reduced, and the hepatic expression of phosphorylated-AMPK and PPAR-α was restored after V9 administration. V9 suppressed the production of inflammatory cytokines (e.g. IL-6, IL-1β, and TNF-α) in HFD-fed rats. The anti-inflammatory effects of V9 was found to be associated with the inhibition of hepatic expression of TLR4, TLR9, NLRP3, and ASC mRNA. Furthermore, the activation of ERK, JNK, AKT and NF-κB were suppressed by V9 treatment. These results indicate that Bifidobacterium lactis V9 improves NAFLD by regulating de novo lipid synthesis and suppressing inflammation through AMPK and TLR-NF-κB pathways, respectively.
脂肪变性和炎症都是非酒精性脂肪性肝病(NAFLD)进展过程中的关键病理事件。益生菌对NAFLD的预防和治疗有益。动物双歧杆菌乳酸亚种V9(V9)是一种新分离出的具有良好益生菌特性的菌株。本研究旨在评估V9对高脂饮食(HFD)诱导的NAFLD大鼠模型肝脏脂肪变性和炎症反应的影响及机制。我们的结果表明,给予V9可显著减轻HFD诱导的丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)水平升高,从而减轻肝脏脂肪变性。补充V9可减少肝脏甘油三酯和游离脂肪酸的积累,同时增加糖原水平。给予V9的HFD大鼠血清葡萄糖水平也降低。同时,V9给药后SREBP-1c和FAS的转录减少,磷酸化-AMPK和PPAR-α的肝脏表达得以恢复。V9抑制了HFD喂养大鼠中炎性细胞因子(如IL-6、IL-1β和TNF-α)的产生。发现V9的抗炎作用与抑制肝脏TLR4、TLR9、NLRP3和ASC mRNA的表达有关。此外,V9处理可抑制ERK、JNK、AKT和NF-κB的激活。这些结果表明,乳酸双歧杆菌V9分别通过AMPK和TLR-NF-κB途径调节从头脂质合成和抑制炎症来改善NAFLD。