Ganoderic acid A ameliorates non‑alcoholic streatohepatitis (NASH) induced by high‑fat high‑cholesterol diet in mice
- Jing Zhu
- Jiexia Ding
- Siying Li
- Jie Jin
Affiliations: Department of Infectious Diseases, The Fourth Clinical College, Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310006, P.R. China
- Published online on: February 24, 2022 https://doi.org/10.3892/etm.2022.11237
Copyright: © Zhu
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Non‑alcoholic steatohepatitis (NASH) is becoming a huge global health problem. Previous studies have revealed that ganoderic acids have hepatoprotective and hypocholesterolemic effects. In the present study, to evaluate the anti‑NASH activity of ganoderic acid A (GAA), male 6‑week‑old C57BL/6J mice were divided into the following four groups, which were administered different diets: Normal diet (ND group), high‑fat high‑cholesterol diet (HFHC group), HFHC diet supplemented with 25 mg/kg/day (GAAL group) or 50 mg/kg/day of GAA (GAAH group). After 12 weeks of GAA treatment, histopathological results revealed that compared with that of the HFHC group, GAA significantly inhibited fat accumulation, steatosis, inflammation and fibrosis in the liver. GAA effectively reduced serum aspartate transaminase and alanine transaminase levels compared with the HFHC model. Furthermore, the endoplasmic reticulum (ER) stress‑responsive proteins, including glucose‑regulated protein 78, phosphorylated (p)‑eukaryotic initiation factor‑2α and p‑JNK, were significantly suppressed by GAA, while ERp57, p‑MAPK and p‑AKT were significantly increased after GAA treatment. Taken together, it was concluded that GAA could resist HFHC diet‑induced NASH. In terms of its underlying mechanism, GAA could improve liver inflammation and fibrosis by inhibiting hepatic oxidative stress and the ER stress response induced by HFHC.