Objective: To explore the specific protective mechanism of 3021 meal replacement powder (MRP) against non-alcoholic fatty liver disease (NAFLD).
Materials and methods: C57BL/6J male mice were divided into four groups: control group, 3021 MRP group, model group and test group. The lipid accumulation and endoplasmic reticulum stress (ERS)-related proteins in hepatocytes of mice were detected by hematoxylin-eosin (HE) staining, oil red O staining and Western blotting.
Results: The expressions of GRP78, GRP94, p-PERK and p-IRE1α were significantly inhibited in test group compared with those in model group. The protein expressions of p-NF-κB, p-JNK, IL-1β, IL-18 and NOX4 in test group were also significantly lower than those in model group. In vivo and in vitro experiments revealed that the body weight and lipid droplet content, and the expressions of ERS-related proteins (including BIP and XBP-1) in liver tissues all significantly declined in model group compared with those in 3021 MRP group.
Conclusion: In conclusion, 3021 MRP can greatly reduce lipid accumulation by inhibiting ERS, oxidative stress and inflammatory response in NAFLD.
Keywords: 3021 meal replacement powder; ERS; Inflammation; NAFLD; Obesity; Oxidative stress; miR-26a.
© 2023 Xie et al.