黄精多糖理化性质及其对D-半乳糖诱导小鼠氧化损伤的保护作用

Study on the Physicochemical Properties of Polysaccharide from Polygonatum sibiricum and Its Protective Effect on D-Galactose-Induced Oxidative Damage in Mice

本研究从黄精根茎部位提取、分离纯化一种均一多糖组分,分析其理化性质和对氧化损伤的保护作用,并探讨其潜在的保护机制。采用水提醇沉、DEAE-纤维素阴离子交换柱与Sephadex G-100凝胶层析柱从黄精根茎提取、分离得到均一多糖组分PSP。采用苯酚硫酸法、间羟基联苯法、高效凝胶渗透色谱和傅里叶红外光谱等分析PSP的理化性质,并通过D-半乳糖诱导氧化损伤小鼠模型探究PSP的体内抗氧化作用。结果表明,PSP的碳水化合物含量为94.42%±14.73%,其分子量为5566.41 Da,含有β型的呋喃环或吡喃环果糖,以及较长的支链和较多的分支。与模型组相比,PSP高剂量组血清、脑组织、肝脏组织的SOD、GSH-Px与T-AOC水平显著升高(P<0.05),MDA水平显著降低(P<0.05);HE染色发现PSP处理组的肝脏损伤明显得到改善,且肝脏中Nrf2和HO-1的表达显著增强(P<0.05)。因此,结果表明黄精多糖PSP可能通过Nrf2/HO-1信号通路保护小鼠的氧化损伤。

In this study,a homogeneous polysaccharide fraction was extracted and purified from the rhizome of Polygonatum sibiricum,its physicochemical properties and protective effect against oxidative damage were analyzed,and its potential protective mechanism was initially explored.The homogeneous polysaccharide(PSP)was obtained by water extraction,alcohol precipitation,and separation on DEAE-52 cellulose and Sephadex G-100 columns.The phenol sulfate method,m-hydroxybiphenyl method,high performance gel permeation chromatography and Fourier infrared spectroscopy were used to analyze the physicochemical properties of PSP.The in vivo antioxidant effects of PSP were investigated in a mouse model of D-galactose induced oxidative damage.The results showed that the carbohydrate content of PSP was 94.42%±14.73%and its molecular weight was 5566.41 Da.PSP was also found to containβ-type furan or pyran fructose,as well as longer branched chains with more branches.Compared with the model group,the levels of SOD,GSH-Px and T-AOC significantly increased(P<0.05),and MDA levels significantly decreased(P<0.05)in serum,brain tissue and liver tissue of the PSP high dose groups,HE staining revealed that liver damage was significantly ameliorated and the expression of Nrf2 and HO-1 protein in the liver was significantly enhanced in the PSP-treated group(P<0.05).It could be concluded that PSP had a protective effect on oxidative damage in mice,and its protective mechanism might be related to the Nrf2/HO-1 signaling pathway.