In this study, the cell-free extracts (CFE) of Lactobacillus acidophilus NX2-6 were utilized to treat oleic acid (OA)-induced hepatic steatosis. It was found that CFE treatment improved lipid metabolism in OA-induced hepatic steatosis model by downregulating several lipogenic genes but increasing expression levels of lipolysis-related genes. In addition, gene expression analysis revealed that CFE treatment promoted mitochondrial biogenesis and fission by upregulating the mRNA levels of PGC-1α, PGC-1β, Sirt1, NRF1, and Fis1. CFE treatment also increased protein expression of p-AMPKα, PGC-1α, ACOX1, and Sirt1 in OA-treated cells, suggesting that CFE possessed ability to improve energy metabolism. Furthermore, CFE treatment also reversed OA-induced oxidative stress by increasing CAT activity and protein level of Nrf-2 as well as reducing protein expression of ATF6, XBP1, GRP78, p50, and p-ERK, indicating that CFE could inhibit endoplasmic reticulum stress and sterile inflammation. Thus, L. acidophilus NX2-6 had potential to fight against NAFLD.

中文翻译：

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来自嗜酸乳杆菌 NX2-6 提取物的油酸处理的 HepG2 细胞能量代谢和炎症的调节机制

在本研究中，嗜酸乳杆菌的无细胞提取物 (CFE)NX2-6 用于治疗油酸 (OA) 诱导的肝脂肪变性。发现 CFE 治疗通过下调几种脂肪生成基因但增加脂肪分解相关基因的表达水平来改善 OA 诱导的肝脂肪变性模型中的脂质代谢。此外，基因表达分析表明，CFE 处理通过上调 PGC-1α、PGC-1β、Sirt1、NRF1 和 Fis1 的 mRNA 水平来促进线粒体生物发生和裂变。CFE 处理还增加了 OA 处理细胞中 p-AMPKα、PGC-1α、ACOX1 和 Sirt1 的蛋白质表达，表明 CFE 具有改善能量代谢的能力。此外，CFE 治疗还通过增加 CAT 活性和 Nrf-2 的蛋白质水平以及降低 ATF6、XBP1、GRP78、p50 和 p-ERK 的蛋白质表达来逆转 OA 诱导的氧化应激，表明 CFE 可以抑制内质网应激和无菌炎症。因此，L. acidophilus NX2-6 具有对抗 NAFLD 的潜力。