Hepatoprotection of Lycii Fructus Polysaccharide against Oxidative Stress in Hepatocytes and Larval Zebrafish

Autor: Chunmei Liu, Xiaofei Zhang, Zihan Zhao, Min Wang, Dawei Qian, Yutian Gu, Xia Zhang, Bowen Qian, Li Yu, Chunlei Xu, Jiazheng Liu, Funing Cao, Jin-Ao Duan, Yichao Yan, Fang Zhang, Sheng Guo
Rok vydání: 2020
Předmět:
0301 basic medicine
Aging
Article Subject
Apoptosis
Oxidative phosphorylation
medicine.disease_cause
Polysaccharide
Protective Agents
Biochemistry
Cell Line
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Non-alcoholic Fatty Liver Disease
Polysaccharides
Nonalcoholic fatty liver disease
Spectroscopy
Fourier Transform Infrared

medicine
Animals
Humans
Viability assay
RNA
Messenger

Zebrafish
chemistry.chemical_classification
QH573-671
Cell Cycle
Cell Biology
General Medicine
Hydrogen Peroxide
Lycium
medicine.disease
digestive system diseases
Disease Models
Animal

Oxidative Stress
030104 developmental biology
Hepatoprotection
chemistry
Gene Expression Regulation
Liver
030220 oncology & carcinogenesis
Larva
Hepatocytes
Thioacetamide
Cytology
Oxidative stress
Research Article
Zdroj: Oxidative Medicine and Cellular Longevity
Oxidative Medicine and Cellular Longevity, Vol 2021 (2021)
ISSN: 1942-0994
Popis: Scavenging of oxidative stress by antioxidants may provide a therapeutic strategy for nonalcoholic fatty liver disease (NAFLD). Increasing evidence is supporting the potential application of natural resourced polysaccharides as promising prevention or treatment strategies against NAFLD. In the current study, an acidic heteropolysaccharide, LFP-a1, was isolated and purified from Lycii fructus with successively hot water refluxing extraction, alcohol precipitation, protein removal, and DEAE-52 cellulose chromatographic separation. LFP-a1 was a complicated structured polysaccharide with an average MW of 4.74 × 104 Da and composed of 6 monosaccharides and 1 uronic acid. Preexposure of LFP-a1 could increase the cell viability and reverse the abnormal oxidative stress though inhibition of mitochondrial-mediated apoptotic pathway and correction of cell cycle progression against H2O2 hepatoxicity in NAFLD model L02 cells. Consistently, in vivo study in thioacetamide- (TAA-) induced NAFLD model zebrafish larvae showed LFP-a1 preserved the liver integrity and alleviated TAA-induced oxidative stress through downregulation of abnormal apoptosis. These observations indicated the hepatoprotective activity of LFP-a1, which may be applied for the prevention or treatment of NAFLD or other oxidative stress-related diseases.
Databáze: OpenAIRE