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目的探讨西洋参皂甙的抗氧化功能及其对环磷酰胺(Cyclophosphamide,CP)所致小鼠遗传损伤的保护作用。方法应用总抗氧化能力(Total Antioxidant Capacity,TAC)和抑制超氧阴离子(O2-)活力试剂盒检测西洋参皂甙的TAC和抑制O2-的活力;水杨酸比色法检测羟自由基(OH-)的清除能力;邻苯三酚自氧化法检测O2-自由基的清除能力。给昆明小鼠每天灌胃不同浓度(10、50、200 mg/kg)的西洋参皂甙,第6天起按25 mg/kg以CP染毒,连续5 d,用试剂盒检测血清谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活性及丙二醛(MDA)的水平;常规Giemsa染色观察小鼠骨髓细胞微核的形成并计算微核形成率;构建小鼠遗传损伤模型,常规Giemsa染色观察小鼠精子畸变程度并计算精子畸变率。结果西洋参皂甙在体外模拟系统中的TAC和抑制O2-生成活力较高,分别达80和160 U/ml,对OH-和O2-的清除率达70%～80%,且呈剂量效应关系;西洋参皂甙干预可显著提高CP染毒小鼠血清中GSH-Px和SOD的活性(P<0.01),降低MDA的水平(P<0.05),拮抗CP对精子和骨髓细胞的损伤作用,西洋参皂甙各剂量组小鼠的精子畸变率和微核形成率与模型组相比,均明显下降(P<0.01)。结论西洋参皂甙具有较强的体内外抗氧化活性,对CP所致小鼠遗传损伤具有明显的保护作用,其机制可能与提高机体的抗氧化能力和增强小鼠的抗诱变能力有关。
Objective To investigate the antioxidant function of ginsenosides and its protective effect on the genetic damage induced by cyclophosphamide (CP) in mice. Methods The total antioxidant capacity (TAC) and the inhibition of superoxide anion (O2-) activity kit were used to detect the TAC of ginsenosides and inhibit the activity of O2-. Salicylic acid colorimetric method was used to detect the hydroxyl radical (OH- ) Scavenging ability; pyrogallol autoxidation method to detect the scavenging capacity of O2-radical. Kunming mice were given ginsenosides at different concentrations (10, 50, 200 mg / kg) daily and CP at 25 mg / kg on the 6th day for 5 consecutive days. Serum glutathione (GSH-Px), superoxide dismutase (SOD) activity and malondialdehyde (MDA) level were measured. The formation of micronuclei in mouse bone marrow cells was observed by conventional Giemsa staining and the rate of micronuclei formation was calculated. Mouse model of genetic damage, conventional Giemsa staining observed sperm aberration in mice and calculate the rate of sperm aberration. Results The ginsenosides had a higher TAC and O2-producing activity in in vitro simulated systems, which reached 80 and 160 U / ml respectively. The clearance rate of OH- and O2- was 70% ~ 80% and dose-dependent. The intervention of ginsenosides could significantly increase the activity of GSH-Px and SOD (P <0.01), decrease the level of MDA (P <0.05), and antagonize the injury of spermatozoa and bone marrow cells in CP-treated mice. The concentrations of ginsenosides Compared with the model group, the sperm aberration rate and micronucleus formation rate in the dose group were significantly decreased (P <0.01). Conclusion Ginsenosides has a strong antioxidant activity in vitro and in vivo, and has a significant protective effect on the genetic damage induced by CP in mice. The mechanism may be related to improving the antioxidant capacity and enhancing the anti-mutagenic ability of mice.