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

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 curre...

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Detalles Bibliográficos
Autores principales: Zhang, Fang, Zhang, Xia, Gu, Yutian, Wang, Min, Guo, Sheng, Liu, Jiazheng, Zhang, Xiaofei, Zhao, Zihan, Qian, Bowen, Yan, Yichao, Yu, Li, Xu, Chunlei, Liu, Chunmei, Cao, Funing, Qian, Dawei, Duan, Jin-ao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7906805/
https://www.ncbi.nlm.nih.gov/pubmed/33680282
http://dx.doi.org/10.1155/2021/3923625
Descripción
Sumario: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 H(2)O(2) 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.