急性肝损伤的发展可能导致肝硬化、肝功能衰竭，甚至肝癌，但目前尚没有有效治疗方法。本研究的目的是探究枸杞多糖（LBPs）对四氯化碳（CCl4）诱导的急性肝损伤的保护作用和治疗机制。实验犬接受1 mL/kg CCl4溶液的腹腔注射，建立急性肝损伤模型。治疗组实验犬口服LBPs（20 mg/kg）。根据显微结构数据，LBPs可以改善CCl4诱导的肝脏结构损伤、过度纤维化和减少线粒体密度。通过抑制Keap1，促进SQSTM1/p62、Nrf2和Nrf2下游的II期解毒基因和蛋白质的产生，并恢复类似过氧化氢酶（CAT）的抗氧化酶活性，LBPs可以恢复和增加肝脏的抗氧化能力。为了减轻线粒体损伤，LBPs还可以增加线粒体呼吸，提高组织三磷酸腺苷（ATP）水平，并重新激活呼吸链复合物I-V。根据血清代谢组学，LBPs对急性肝损伤的治疗影响主要是通过调控脂质代谢途径实现的。9-羟基十八碳二烯酸（9-HODE）、溶血磷脂酸基胆碱（LysoPC/LPC）和磷脂酰乙醇胺（PE）可能是急性肝损伤的潜在指标。本研究证实LBPs是一种有效的肝保护药物，可以通过降低氧化应激、修复线粒体损伤和调节代谢途径来治愈急性肝损伤。

The development of acute liver injury can result in liver cirrhosis, liver failure, and even liver cancer, yet there is currently no effective therapy for it. The purpose of this study was to investigate the protective effect and therapeutic mechanism of Lyciumbarbarum polysaccharides (LBPs) on acute liver injury induced by carbon tetrachloride (CCl4). To create a model of acute liver injury, experimental canines received an intraperitoneal injection of 1 mL/kg of CCl4 solution. The experimental canines in the therapy group were then fed LBPs (20 mg/kg). CCl4-induced liver structural damage, excessive fibrosis, and reduced mitochondrial density were all improved by LBPs, according to microstructure data. By suppressing Kelch-like epichlorohydrin (ECH)-associated protein 1 (Keap1), promoting the production of sequestosome 1 (SQSTM1)/p62, nuclear factor erythroid 2-related factor 2 (Nrf2), and phase II detoxification genes and proteins downstream of Nrf2, and restoring the activity of anti-oxidant enzymes like catalase (CAT), LBPs can restore and increase the antioxidant capacity of liver. To lessen mitochondrial damage, LBPs can also enhance mitochondrial respiration, raise tissue adenosine triphosphate (ATP) levels, and reactivate the respiratory chain complexes I‒V. According to serum metabolomics, the therapeutic impact of LBPs on acute liver damage is accomplished mostly by controlling the pathways to lipid metabolism. 9-Hydroxyoctadecadienoic acid (9-HODE), lysophosphatidylcholine (LysoPC/LPC), and phosphatidylethanolamine (PE) may be potential indicators of acute liver injury. This study confirmed that LBPs, an effective hepatoprotective drug, may cure acute liver injury by lowering oxidative stress, repairing mitochondrial damage, and regulating metabolic pathways.