Dihydromyricetin Ameliorates Exercise-Induced Acute Hepatic Dysfunction and Inflammation in Association with the Restoration of the Th17/Treg Balance in Mice
- 1Research Center for Nutrition and Food Safety, Chongqing Key Laboratory of Nutrition and Health, Institute of Military Preventive Medicine, Army Medical University, Chongqing 400038, China
Abstract
Exercise induces acute hepatic dysfunction and inflammation, a condition with currently limited treatment modalities. Dihydromyricetin (DHM) may protect the liver, but its role in exercise-related hepatic dysfunction and inflammation remains to be elucidated. In this work, we investigated whether DHM intervention is associated with the restoration of the T helper 17 (Th17)/regulatory T (Treg) balance in these exercise-induced hepatic disorders.Exhaustive treadmill running was performed on male C57BL/6 mice (8 weeks old, 20–22 g) to establish a mouse model of acute hepatic dysfunction and inflammation. Mice were then administered DHM (400 mg/kg/day by oral gavage for 6 consecutive days, concurrently with the exercise protocol), DHM + recombinant interleukin-17A (IL-17A) (rIL-17A; 100 ng/day, i.p., on Days 1–4 of the exercise protocol), or DHM + anti-CD25 monoclonal antibody (aCD25 mAb; 400 µg, i.p., on the second day of acclimatization and the third day of the exercise protocol). After acute exercise, livers were harvested for histopathological analysis, protein expression profiling, and immune cell population analysis. Acute exercise induced histological changes in the liver with infiltration of inflammatory cells, elevated serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT), and increased hepatic Th17 cells and the Th17/Treg ratio, without significantly altering Treg cells, compared with the non-exercise group. DHM administration attenuated these changes, and this protective effect was associated with the restoration of the Th17/Treg balance. Administration of rIL-17A or aCD25 mAb blunted the protective effect of DHM. Our results suggest that DHM administration may serve as a potential protective strategy against exercise-induced transient hepatic dysfunction and inflammation, in association with the restoration of the Th17/Treg balance in mice.
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BibTeX
@article{zhang2026dihydromyricetin,
title = {{Dihydromyricetin Ameliorates Exercise-Induced Acute Hepatic Dysfunction and Inflammation in Association with the Restoration of the Th17/Treg Balance in Mice}},
author = {Yong Zhang and Jing Yue and Qianyong Zhang and Long Yi},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = nov,
doi = {10.3390/ijms27219846},
url = {https://www.mdpi.com/1422-0067/27/21/9846},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Dihydromyricetin Ameliorates Exercise-Induced Acute Hepatic Dysfunction and Inflammation in Association with the Restoration of the Th17/Treg Balance in Mice
AU - Yong Zhang
AU - Jing Yue
AU - Qianyong Zhang
AU - Long Yi
PY - 2026
DA - 2026/11/03
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219846
UR - https://www.mdpi.com/1422-0067/27/21/9846
AB - Exercise induces acute hepatic dysfunction and inflammation, a condition with currently limited treatment modalities. Dihydromyricetin (DHM) may protect the liver, but its role in exercise-related hepatic dysfunction and inflammation remains to be elucidated. In this work, we investigated whether DHM intervention is associated with the restoration of the T helper 17 (Th17)/regulatory T (Treg) balance in these exercise-induced hepatic disorders.Exhaustive treadmill running was performed on male C57BL/6 mice (8 weeks old, 20–22 g) to establish a mouse model of acute hepatic dysfunction and inflammation. Mice were then administered DHM (400 mg/kg/day by oral gavage for 6 consecutive days, concurrently with the exercise protocol), DHM + recombinant interleukin-17A (IL-17A) (rIL-17A; 100 ng/day, i.p., on Days 1–4 of the exercise protocol), or DHM + anti-CD25 monoclonal antibody (aCD25 mAb; 400 µg, i.p., on the second day of acclimatization and the third day of the exercise protocol). After acute exercise, livers were harvested for histopathological analysis, protein expression profiling, and immune cell population analysis. Acute exercise induced histological changes in the liver with infiltration of inflammatory cells, elevated serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT), and increased hepatic Th17 cells and the Th17/Treg ratio, without significantly altering Treg cells, compared with the non-exercise group. DHM administration attenuated these changes, and this protective effect was associated with the restoration of the Th17/Treg balance. Administration of rIL-17A or aCD25 mAb blunted the protective effect of DHM. Our results suggest that DHM administration may serve as a potential protective strategy against exercise-induced transient hepatic dysfunction and inflammation, in association with the restoration of the Th17/Treg balance in mice.
SN - 1422-0067
ER -