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
Jiangsu Collaborative Innovation Center of Chinese Medicinal Resources Industrialization, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China.
School of Pharmacy, Ningxia Medical University, Yinchuan 750004, China.
Oxid Med Cell Longev. 2021 Feb 18;2021:3923625. doi: 10.1155/2021/3923625. eCollection 2021.
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 HO hepatoxicity in NAFLD model L02 cells. Consistently, 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.
抗氧化剂清除氧化应激可能为非酒精性脂肪性肝病（NAFLD）提供一种治疗策略。越来越多的证据支持将天然来源的多糖作为预防或治疗NAFLD的有前景的策略。在本研究中，通过依次热水回流提取、乙醇沉淀、去除蛋白质和DEAE-52纤维素柱色谱分离，从枸杞中分离并纯化出一种酸性杂多糖LFP-a1。LFP-a1是一种结构复杂的多糖，平均分子量为4.74×104 Da，由6种单糖和1种糖醛酸组成。预先暴露LFP-a可以提高细胞活力，并通过抑制线粒体介导的凋亡途径和纠正细胞周期进程来逆转异常的氧化应激，从而对抗NAFLD模型L02细胞中的HO肝毒性。同样，在硫代乙酰胺（TAA）诱导的NAFLD模型斑马鱼幼虫中的研究表明，LFP-a1通过下调异常凋亡来维持肝脏完整性并减轻TAA诱导的氧化应激。这些观察结果表明LFP-a1具有肝脏保护活性，可用于预防或治疗NAFLD或其他氧化应激相关疾病。
