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Probiotic Bifidobacterium lactis V9 attenuates hepatic steatosis and inflammation in rats with non-alcoholic fatty liver disease.
AMB Express ( IF 3.7 ) Pub Date : 2020-05-29 , DOI: 10.1186/s13568-020-01038-y
Yan Yan 1 , Chunyan Liu 1 , Shimin Zhao 1 , Xinxu Wang 1 , Jinling Wang 2 , Heping Zhang 3 , Yuzhen Wang 1 , Guofen Zhao 1
Affiliation  

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.



中文翻译:

益生菌乳酸双歧杆菌V9可减轻非酒精性脂肪肝大鼠的肝脂肪变性和炎症。

脂肪变性和炎症都是非酒精性脂肪肝疾病(NAFLD)进展中的关键病理事件。益生菌对预防和治疗NAFLD有益。动物双歧杆菌亚种。乳酸菌V9(V9)是具有良好益生菌特性的新分离菌株。这项研究旨在评估V9对高脂饮食(HFD)诱导的NAFLD大鼠模型中肝脂肪变性和炎症反应的作用和机制。我们的结果表明,V9的使用显着减轻了HFD诱导的丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)水平的升高,从而减轻了肝脂肪变性。V9补充剂减少了肝甘油三酯和游离脂肪酸的积累,同时增加了糖原的水平。用V9注射的HFD大鼠的血清葡萄糖水平也降低了。同时,施用V9后,SREBP-1c和FAS的转录减少,并且磷酸化的AMPK和PPAR-α的肝表达恢复。V9抑制了喂食HFD的大鼠中炎性细胞因子(例如IL-6,IL-1β和TNF-α)的产生。发现V9的抗炎作用与抑制TLR4,TLR9,NLRP3和ASC mRNA的肝表达有关。此外,通过V9处理抑制了ERK,JNK,AKT和NF-κB的活化。这些结果表明乳酸双歧杆菌V9通过调节新生脂质合成并分别通过AMPK和TLR-NF-κB途径抑制炎症来改善NAFLD。

更新日期:2020-05-29
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