TY  - JOUR
AU  - CAI, Wenwen
AU  - GE, Xiaodong
AU  - LI, Na
AU  - GONG, Shiyu
AU  - LIU, Bin
AU  - CHEN, Fuquan
AU  - ZENG, Feng
PY  - 2022
TI  - Protective Effect of Oyster Protein Hydrolysate on Chronic Alcoholic Liver Injury in Mice
JO  - Food Science
SN  - 1002-6630
SP  - 147
EP  - 155
VL  - 43
IS  - 17
AB  - This study aimed to explore the hepatoprotective effect of an enzymatic hydrolysate from oyster meat on chronic alcoholic liver injury in mice. After intervention with the hydrolysate, the serum levels of alaninetransaminase (ALT) activity, aspartate aminotransferase (AST) activity and total bile acid (TBA) concentration, liver index, and the contents of triglyceride (TG) and malondialdehyde (MDA) in the liver of mice with chronic alcoholic liver injury were measured, liver histomorphological changes were examined, and the mRNA transcription level of related genes in the liver and the changes of the gut microflora structure were analyzed. The results demonstrated that compared with the model group, the enzymatic hydrolysate at high and low doses significantly decreased the activity of serum ALT and AST and liver TG and MDA contents (P < 0.05, P < 0.01), but increased liver glutathione (GSH) content (P < 0.01). TBA content was significantly lower in the high-dose hydrolysate group (P < 0.05). The hydrolysate at high and low doses alleviated alcohol-induced liver damage in mice, and significantly down-regulated the mRNA transcription levels of the genes encoding toll-like recepror 4 (TLR4), tumor necrosis factor α (TNF-α), and nuclear factor-kappa B (NF-κB) (P < 0.05). The hydrolysate increased the abundance of Firmicutes as well as Lactobacillus and Alistipes, and reduced the abundance of Bacteroidetes in the gut of mice. In conclusion, the enzymatic hydrolysate can protect against chronic alcoholic liver injury in mice through reducing the activity of AST and ALT, and the contents of TG, MDA and TBA, increasing GSH content, down-regulating the mRNA transcription levels of TLR4, NF-κB and TNF-α, and changing the structure of the gut microflora.
UR  - https://doi.org/10.7506/spkx1002-6630-20210720-228
DO  - 10.7506/spkx1002-6630-20210720-228