在明确猴头菇多糖的理化特性的基础上，探讨其神经保护作用机制。以猴头菇子实体为原料，水提醇沉制备猴头菇粗多糖，DEAE-52纤维素层析柱和Sephacry1 S-300 HR色谱柱进行分离纯化，获得猴头菇精多糖组份（HEP），SEM、FT-IR分析多糖的形貌及结构特性，PMP柱前衍生法明确其单糖组分。自由基清除活性实验分析HEP 的抗氧化活性，构建H2O2胁迫诱导的PC12细胞损伤模型，探索HEP的神经保护活性及其作用机制。结果显示：HEP精多糖得率为1.07%，分离获得三个多糖片段，颗粒状态不均，主要由甘露糖、木糖、葡萄糖、半乳糖醛酸和岩藻糖组成，FT-IR明确HEP异头碳为β构型。通过HEP对DPPH自由基、羟基自由基、超氧阴离子清除活性测定发现其对三种自由基都表现出清除活性，IC50 值分别为1.61、2.23和2.89 mg/mL。此外，HEP对H2O2胁迫损伤的PC12细胞具有保护作用，其作用机理涉及细胞内源性抗氧化酶活性重塑和降低Caspases-3的活性。HEP具有抗氧化活性，对氧化损伤引发的细胞凋亡有保护作用，可能成为治疗或预防神经退行性疾病的一种新策略。

Upon identifying the physicochemical properties of polysaccharides extracted from Hericium erinaceus (HEP), the neural protective mechanisms were investigated. HEP was prepared from the fruiting bodies of Hericium erinaceus via aqueous extraction and alcohol precipitation. Separation and purification were achieved using DEAE-52 cellulose chromatography columns and Sephacryl S-300 HR chromatography columns. Scanning electron microscopy (SEM) and Fourier-transform infrared (FT-IR) spectroscopy were used to analyze the morphology and structural characteristics of the polysaccharides. The monosaccharide composition was determined via pre-column derivatization with 1-phenyl-3-methyl-5-pyrazolone (PMP). Free radical scavenging assays were conducted to analyze the antioxidant activity of HEP. A H2O2-induced PC12 cell model was established to explore the neuroprotective activity of HEP and its underlying mechanisms. The results demonstrated that HEP had a yield of 1.07% and could be divided into three polysaccharide fractions. These fractions exhibited non-uniform granular structures and primarily consisted of mannose, xylose, glucose, galacturonic acid, and fucose. FTIR analysis confirmed the β-configuration of HEP. HEP displayed scavenging activity against DPPH, hydroxyl radicals, and superoxide anions, with IC50 values of 1.61 mg/mL, 2.23 mg/mL, and 2.89 mg/mL, respectively. Furthermore, HEP exhibited a protective effect on H2O2-induced PC12 cell damage. The mechanism of action involved endogenous antioxidant enzyme activity remodeling and Caspase-3 activity reduction. HEP demonstrated antioxidant activity and protected against oxidative damage-induced apoptosis, suggesting its potential as a novel strategy for the treatment or prevention of neurodegenerative diseases.

四川省自然科学基金项目（22NSFSC3818）