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Research Article | Open Access | Just Accepted

Schisandrin A Ameliorates Endoplasmic Reticulum Stress Mediated Apoptosis in Metabolic Associated Fatty Liver Disease

Jing Zhou1,2,#Ying Shi1,2,#Zuzhen Bao2Mengmeng Luo1,2Jie Li2,6Marwan M. A. Rashed2Suowen Xu4Jianhua Yang5Hong Duan1,2()Henggui Hu3()Kefeng Zhai1,2()

1 College of Biological and Food Engineering, Anhui Polytechnic University, Wuhu, Anhui 241000, China

2 School of Biological and Food Engineering, Engineering Research Center for Development and High Value Utilization of Genuine Medicinal Materials in North Anhui Province, Suzhou University, Suzhou, Anhui 234000, China

3 General Clinical Research Center, Anhui Wanbei Coal-Electricity Group General Hospital,Suzhou 234000, China

4 Department of Endocrinology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei230000, China

5 Department of Pharmacy, The First Affiliated Hospital of Xinjiang Medical University, Xinjiang Key Laboratory of Clinical Drug Research, Urumqi 830011, China

6 College of Pharmacy,Wannan Medical College,Wuhu 241000, China

# Authors contributed equally

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Abstract

Background: Metabolic associated fatty liver disease (MAFLD) is closeky linked to metabolic disorders and lack of effective therapeutic options. Schisandrin A (SA), derived from the traditional Chinese medicinal herb Schisandra, has shown liver-protective properties. SA may counteract MAFLD by modulating endoplasmic reticulum stress (ERS) and inhibiting apoptosis. This study aimed to investigate the protective effects of SA on high-fat diet-induced MAFLD in C57BL/6 mice. The study also sought to elucidate the underlying mechanisms, focusing on the ERS signaling pathway and apoptosis.

Methods: MAFLD mice models were induced with a high-fat diet and divided into control, model, SA intervention (various dosages), atorvastatin positive control, and ERS inhibitor combined with SA intervention groups. serum lipid profiles, liver enzymes, and liver histopathology were assessed. Western blot, immunofluorescence, and TUNEL assay were used to evaluate ERS and apoptosis-related protein expression.

Results: SA intervention markedly enhanced serum lipid profiles and reduced liver enzyme levels. The histopathological alterations observed in the model group were significantly mitigated by SA treatment. Western blot analysis revealed that SA effectively modulated the expression levels of proteins associated with ERS and apoptosis. Furthermore, immunofluorescence and TUNEL assay results substantiated SA's regulatory influence on ERS and apoptotic pathways.

Conclusion: SA effectively improved dyslipidemia and hepatic lipid metabolism abnormalities. It reduced hepatic lipid deposition and pathological damage in MAFLD mice induced by a high-fat diet. The mechanism of action may involve the regulation of the ERS signaling pathway, thereby protecting cells from apoptosis.

Food Science and Human Wellness
Cite this article:
Zhou J, Shi Y, Bao Z, et al. Schisandrin A Ameliorates Endoplasmic Reticulum Stress Mediated Apoptosis in Metabolic Associated Fatty Liver Disease. Food Science and Human Wellness, 2025, https://doi.org/10.26599/FSHW.2025.9250472
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