黄芪多糖对表柔比星致小鼠表皮溃疡中氧化应激的调节作用

Regulation of astragulas polysaccharide to oxidative stress in mice with dermal ulcer induced by Epirubicin

目的探讨黄芪多糖对表柔比星致小鼠表皮溃疡及创面氧化应激反应的影响。方法BALB/c雄性小鼠310只,表柔比星2g/L皮内注射制备慢性皮肤溃疡动物模型,随机分为模型组,黄芪多糖高、低剂量组,重组人表皮细胞生长因子组(简称生长因子组)、Trolox组。苏木素伊红、Masson、天狼星红染色观察创面组织形态学及胶原变化,采用图像软件分析创面面积;分光光度计法检测创面组织超氧化物歧化酶(SOD)、丙二醛(MDA)水平。结果黄芪多糖能够促进疮面结痂,缩短溃疡愈合时间,平均愈合时间由模型组的(29.75±3.58)d缩短至(23.25±4.80)d,并且少于生长因子组(26.29±4.12)d,能够促进溃疡创面的表皮细胞及胶原修复。造模后13d疮面组织氧化应激损伤最明显,SOD活力为(9.69±1.99)U/mg,MDA水平为(15.48±3.72)nmol/mg;黄芪多糖高、低剂量治疗后SOD活力分别提高为(14.56±0.83)U/mg、(12.07±1.59)U/mg;MDA水平分别降低为(14.32±0.83)nmol/mg和(11.14±1.59)nmol/mg,与对照组比较差异显著,P<0.05。造模后27d疮面组织基本愈合,各组SOD活力和MDA水平都接近正常水平。结论黄芪多糖能够促进小鼠皮肤溃疡创面结痂,缩短愈合时间;其作用机制与其能够促进疮面表皮细胞及胶原修复,降低创面组织脂质过氧化损伤,提高抗氧化能力有关。

Objective To discuss the effect of astragulas polysaccharide （APS） on oxidative stress in mice with dermal ulcer induced by Epirubicin. Methods The model of dermal ulcer was established in 310 male Balb/c mice by intradermal injection of 2 g/L Epirubicin. Then the mice were randomly divided into 5 groups, including the model group, high-dose APS group, low-dose APS group, rhEGF group and Trolox group. The changes of histomorphology and collagen were observed by staining methods of HE, MASSON and red Sirius in wound. The wound area was analyzed by digital image software. SOD activity and MDA level in wound were detected by spectrophotometry. Results APS accelerated wound healing speed and shortened healing time. The average healing time was from 29.75 ± 3.58 days in the model group to 23.25 ±4.80 days, which was less than that of the rhEGF group （26.29 ±4.12 days）. APS also improved the repair of epidermis and collagen. The oxidative injuries in wound were most obvious 13 days after Epirubicin injection showed as follows ： SOD activity was （9.69 ±1.99 ） U/mg and MDA level was （15.48 ± 3.72） nmol/mg. After the treatment in the high-dose of APS and low-dose APS groups SOD activity was increased to （ 14.56 ±0.83 ） U/mg and （ 12.07±1.59） U/mg respectively and the MDA level was deceased to （ 14.32 ±0.83） nmol/mg and （ 11.14±1.59） nmol/mg respectively. There was a significant difference （ P 〈 0.05 ） compared to those of the model group. The wound was healed basically 27 days after the modeling. SOD activity and MDA level in each group were near to normal level. Conclusion APS can accelerate wound healing speed and shorten healing time. The mechanism may be related to that it can improve the repair of epidermis and collagen, decrease lipoperoxidation injuries and increase antioxidant activity in wound.