【摘要】 目的：观察三七总皂苷(PNS)结合细胞穿透肽Tat(47-57)对骨折的愈合作用，并探讨其可能机制。方法：研究选取成年雄性SD大鼠建立骨折实验动物模型，实验动物随机分为四组：空白对照组、外用三七总皂苷组(PNS外用组)、外用三七总皂苷和细胞穿透肽联合组(Tat-PNS外用组)、口服三七总皂苷组(PNS口服组)。给药14d后，检测骨折病灶局部的抗氧化SOD酶活性，同时取骨折病灶局部进行病理切片分析，对比和分析各给药组对实验大鼠骨折愈合过程的影响程度。结果：与空白对照组对比，PNS外用组对大鼠骨折愈合无明显的疗效，可能与PNS无法有效透皮吸收，并在病灶局部富集有效浓度有关。Tat-PNS外用组能够明显增加病灶局部的SOD酶活性(P<0.05),而且病理切片显示骨折处恢复状况良好，其促进骨折病灶处愈合的效果与PNS口服组效果基本一致。结论：三七总皂苷与细胞穿透肽Tat(47-57)联合经皮给药能够明显促进骨折愈合，其作用机制可能与提高骨折病灶局部的抗氧化力，增强骨形态发生蛋白BMP-2的表达有关。更多还原

【Abstract】 Objective:To observe the effect of Panax notoginseng saponins(PNS) combined with cell penetrating peptide Tat(47-57) on fracture healing and explore its possible mechanism.Methods:Adult male SD rats were selected to establish the experimental animal model of fracture, and the experimental animals were randomly divided into four groups: blank control group, Panax notoginseng saponins for external use group(PNS for external use group),Panax notoginseng saponins group combined with cell penetrating peptide group(Tat-PNS group), and Panax notoginseng saponins oral treatment group(PNS oral treatment group).After 14 days of administration, the activity of antioxidant SOD enzyme in the local fracture lesions was detected, and the pathological sections of the local fracture lesions were analyzed to compare and analyze the effect of each administration groups on the fracture healing process of experimental rats.Results:Compared with blank control group, PNS for external use group had no obvious curative effect on fracture healing in rats, which may be related to the inability of PNS to effectively absorb through the skin and local enrichment of effective concentration in the lesion. Tat-PNS group can significantly increase the activity of SOD enzyme in local lesions(P<0.05),and the results of pathological section analysis showed that the fracture site recovered well, and the effect of Tat-PNS group on promoting the healing of fracture site was basically the same as that of PNS oral treatment group.Conclusion:The combination of Panax notoginseng saponins and cell penetrating peptide Tat(47-57) can significantly promote fracture healing.Its mechanism may be related to improving the local antioxidant capacity of fracture lesions and enhancing the expression of bone morphogenetic protein BMP-2.更多还原