Ursolic Acid in Hippophae rhamnoides L. Protects against Alcohol-Induced Hepatic Injury by Alleviating Inflammatory Response and Regulating Fas/FasL Activation
7 affiliations
- 1School of Pharmacy, Baotou Medical College, Baotou 014040, China
- 2School of Public Health, Baotou Medical College, Baotou 014040, China
- 3Center for Disease Control and Prevention of Chinese PLA, Beijing 100071, China
- 4Department of Orthopedics, The First Affiliated Hospital of Baotou Medical College, Baotou 014010, China
- 5Institute of Food Nutrition and Health, Baotou Medical College, Baotou 014040, China
- 6Translational Medicine Center, Baotou Medical College, Baotou 014040, China
- 7School of Basic Medicine and Forensic Medicine, Baotou Medical College, Baotou 014040, China
Abstract
Alcoholic liver disease (ALD), a form of liver damage due to excessive alcohol consumption, has become one of the major causes of chronic liver disease and a significant public health concern, according to a World Health Organization report on alcohol and health. However, apart from abstinence, there are few targeted adjunctive therapies for ALD. The study was designed to explore the potential protective effects of ursolic acid (UA) from Hippophae rhamnoides L. against ALD in rats and to analyze the mechanisms associated with the death receptor-mediated exogenous pathway. After alcohol modeling and UA treatment, blood was sampled and liver and kidney tissues were collected for testing various indicators. UA significantly improved the hepatic histological structure and decreased serum biochemical indices and interleukin-1β and tumor necrosis factor-α levels due to alcohol-induced liver damage. UA inhibited the overexpression of the nuclear factor kappa B subunit p65, phosphorylated inhibitor of nuclear factor kappa B, cyclooxygenase-2, Fas cell surface death receptor (Fas), Fas ligand, apoptosis-related cysteine peptidase (caspase)-8, and apoptosis-related caspase-3. Therefore, our findings suggest that UA from H. rhamnoides could improve alcoholic liver injury by suppressing the inflammatory response, inhibiting hepatocyte apoptosis, and modulating the death receptor-mediated extrinsic pathway. Thus, UA could be developed into a potential bioactive material to prevent hepatic injury induced by ethanol.
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BibTeX
@article{zhu2026ursolic,
title = {{Ursolic Acid in Hippophae rhamnoides L. Protects against Alcohol-Induced Hepatic Injury by Alleviating Inflammatory Response and Regulating Fas/FasL Activation}},
author = {Wei Zhu and Kexin Li and Wenlong Zhang and Ruili Hou and Mengqi Shi and Xiaoe Jia and Min Jin and Na Ge},
journal = {Preventive Nutrition and Food Science},
year = {2026},
month = oct,
doi = {10.3746/pnf.2026.078},
url = {https://doi.org/10.3746/pnf.2026.078},
note = {CC BY-NC 4.0},
}
RIS
TY - JOUR
TI - Ursolic Acid in Hippophae rhamnoides L. Protects against Alcohol-Induced Hepatic Injury by Alleviating Inflammatory Response and Regulating Fas/FasL Activation
AU - Wei Zhu
AU - Kexin Li
AU - Wenlong Zhang
AU - Ruili Hou
AU - Mengqi Shi
AU - Xiaoe Jia
AU - Min Jin
AU - Na Ge
PY - 2026
DA - 2026/10/19
JO - Preventive Nutrition and Food Science
DO - 10.3746/pnf.2026.078
UR - https://doi.org/10.3746/pnf.2026.078
AB - Alcoholic liver disease (ALD), a form of liver damage due to excessive alcohol consumption, has become one of the major causes of chronic liver disease and a significant public health concern, according to a World Health Organization report on alcohol and health. However, apart from abstinence, there are few targeted adjunctive therapies for ALD. The study was designed to explore the potential protective effects of ursolic acid (UA) from Hippophae rhamnoides L. against ALD in rats and to analyze the mechanisms associated with the death receptor-mediated exogenous pathway. After alcohol modeling and UA treatment, blood was sampled and liver and kidney tissues were collected for testing various indicators. UA significantly improved the hepatic histological structure and decreased serum biochemical indices and interleukin-1β and tumor necrosis factor-α levels due to alcohol-induced liver damage. UA inhibited the overexpression of the nuclear factor kappa B subunit p65, phosphorylated inhibitor of nuclear factor kappa B, cyclooxygenase-2, Fas cell surface death receptor (Fas), Fas ligand, apoptosis-related cysteine peptidase (caspase)-8, and apoptosis-related caspase-3. Therefore, our findings suggest that UA from H. rhamnoides could improve alcoholic liver injury by suppressing the inflammatory response, inhibiting hepatocyte apoptosis, and modulating the death receptor-mediated extrinsic pathway. Thus, UA could be developed into a potential bioactive material to prevent hepatic injury induced by ethanol.
SN - 2287-1098
SN - 2287-8602
ER -