Lu Jing, Shataer Dilireba, Yan Huizhen, Dong Xiaoxiao, Zhang Minwei, Qin Yanan, Cui Jie, Wang Liang
Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi 830046, China.
College of Food Science and Light Industry, Nanjing Tech University, Nanjing 211816, China.
Foods. 2024 Sep 21;13(18):2992. doi: 10.3390/foods13182992.
In recent years, the prevalence of non-alcoholic fatty liver disease (NAFLD) has risen annually, yet due to the intricacies of its pathogenesis and therapeutic challenges, there remains no definitive medication for this condition. This review explores the intricate relationship between the intestinal microbiome and the pathogenesis of NAFLD, emphasizing the substantial roles played by and . These probiotics manipulate lipid synthesis genes and phosphorylated proteins through pathways such as the AMPK/Nrf2, LPS-TLR4-NF-κB, AMPKα/PGC-1α, SREBP-1/FAS, and SREBP-1/ACC signaling pathways to reduce hepatic lipid accumulation and oxidative stress, key components of NAFLD progression. By modifying the intestinal microbial composition and abundance, they combat the overgrowth of harmful bacteria, alleviating the inflammatory response precipitated by dysbiosis and bolstering the intestinal mucosal barrier. Furthermore, they participate in cellular immune regulation, including CD4 T cells and Treg cells, to suppress systemic inflammation. and also modulate lipid metabolism and immune reactions by adjusting gut metabolites, including propionic and butyric acids, which inhibit liver inflammation and fat deposition. The capacity of probiotics to modulate lipid metabolism, immune responses, and gut microbiota presents an innovative therapeutic strategy. With a global increase in NAFLD prevalence, these insights propose a promising natural method to decelerate disease progression, avert liver damage, and tackle associated metabolic issues, significantly advancing microbiome-focused treatments for NAFLD.
近年来，非酒精性脂肪性肝病（NAFLD）的患病率逐年上升，但由于其发病机制复杂且治疗具有挑战性，目前尚无针对该病症的确切药物。本综述探讨了肠道微生物群与NAFLD发病机制之间的复杂关系，强调了[具体益生菌名称1]和[具体益生菌名称2]所起的重要作用。这些益生菌通过AMPK/Nrf2、LPS-TLR4-NF-κB、AMPKα/PGC-1α、SREBP-1/FAS和SREBP-1/ACC信号通路等途径操纵脂质合成基因和磷酸化蛋白，以减少肝脏脂质积累和氧化应激，而这两者是NAFLD进展的关键组成部分。通过改变肠道微生物组成和丰度，它们对抗有害细菌的过度生长，减轻由生态失调引发的炎症反应并加强肠道黏膜屏障。此外，它们参与细胞免疫调节，包括CD4 T细胞和调节性T细胞，以抑制全身炎症。[具体益生菌名称1]和[具体益生菌名称2]还通过调节肠道代谢产物，包括丙酸和丁酸，来调节脂质代谢和免疫反应，这些代谢产物可抑制肝脏炎症和脂肪沉积。益生菌调节脂质代谢、免疫反应和肠道微生物群的能力提出了一种创新的治疗策略。随着全球NAFLD患病率的增加，这些见解提出了一种有前景的天然方法来减缓疾病进展、避免肝脏损伤并解决相关代谢问题，显著推进了针对NAFLD的以微生物群为重点的治疗方法。
