Liang Yuxuan, Wang Zhuo, Li Rui, Zhong Saiyi, Liu Xiaofei, Chen Jianping
College of Food Science and Technology Guangdong Ocean University, Guangdong Provincial Key Laboratory of Aquatic Product Processing and Safety, Guangdong Provincial Engineering Technology Research Center of Seafood, Guangdong Province Engineering Laboratory for Marine Biological Products, Key Laboratory of Advanced Processing of Aquatic Product of Guangdong Higher Education Institution Zhanjiang China.
Food Sci Nutr. 2024 Dec 1;12(12):10913-10923. doi: 10.1002/fsn3.4632. eCollection 2024 Dec.
The study aimed to explore the protective impact of polysaccharide derived from (Turner) C. Agardh (SHP) against ethanol-induced injury in LO2 hepatocytes, along with its potential mechanism of action. A model of alcoholic injury in LO2 cells was established to assess the shielding effect of SHP against liver injury induced by alcohol. Treatment with 800 mmol/L ethanol for 6 h was selected for the construction of the hepatocyte injury model. Compared with those in the alcohol model group, the survival rate of LO2 cells in the SHP treatment group was significantly greater. When the concentration of SHP reached 60 μg/mL, the cell viability increased to 89.17% ± 3.58%. Moreover, SHP treatment significantly reduced the level of intracellular reactive oxygen species (ROS), increased the levels of intracellular glutathione (GSH), lactate dehydrogenase (LDH), and catalase (CAT), reduced the level of malondialdehyde (MDA), and prevented the leakage of intrahepatic enzymes (aspartate aminotransferase (AST) and alanine transaminase (ALT)) to protect LO2 cells from alcohol-induced injury. Moreover, at a concentration of 60 μg/mL, SHP inhibited the ethanol-induced reduction in the protein expressions of Nrf2, HO-2, and GCLC, indicating its potential to modulate the antioxidant system to restore the homeostatic state, consequently shielding the liver from peroxidative damage induced by alcohol. These results propose that SHP exhibits a protective role against oxidative damage in LO2 cells and holds promise as a novel natural hepatoprotective agent for averting liver injury.
本研究旨在探讨来源于（Turner）C. Agardh的多糖（SHP）对乙醇诱导的LO2肝细胞损伤的保护作用及其潜在作用机制。建立LO2细胞酒精损伤模型，以评估SHP对酒精诱导的肝损伤的保护作用。选择用800 mmol/L乙醇处理6小时来构建肝细胞损伤模型。与酒精模型组相比，SHP处理组的LO2细胞存活率显著更高。当SHP浓度达到60 μg/mL时，细胞活力增加到89.17%±3.58%。此外，SHP处理显著降低细胞内活性氧（ROS）水平，增加细胞内谷胱甘肽（GSH）、乳酸脱氢酶（LDH）和过氧化氢酶（CAT）水平，降低丙二醛（MDA）水平，并防止肝内酶（天冬氨酸转氨酶（AST）和丙氨酸转氨酶（ALT））泄漏，从而保护LO2细胞免受酒精诱导的损伤。此外，在浓度为60 μg/mL时，SHP抑制乙醇诱导的Nrf2、HO-2和GCLC蛋白表达降低，表明其有调节抗氧化系统以恢复内稳态的潜力，从而保护肝脏免受酒精诱导的过氧化损伤。这些结果表明，SHP对LO2细胞氧化损伤具有保护作用，有望成为一种新型天然肝保护剂来避免肝损伤。
