Anti-aging effect of adipose-derived stem cells in a mouse model of skin aging induced by D-galactose.
Anti-aging effect of adipose-derived stem cells in a mouse model of skin aging induced by D-galactose.
复制标题
脂肪干细胞在 D-半乳糖诱导的皮肤老化小鼠模型中的抗衰老作用
DOI：
10.1371/journal.pone.0097573
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Lu F
中科院分区：
文献类型：
--
作者：
Zhang S;Dong Z;Peng Z;Lu F
糖基化产物在缓慢更新的组织（包括皮肤）衰老过程中积累，并被认为是皮肤衰老过程的重要机制。脂肪源性细胞在临床上被广泛用于治疗缺血性疾病和促进伤口愈合。有趣的是，脂肪源性干细胞（ASC）在抗衰老治疗中也是有效的，尽管其作用的机制仍然未知。本研究的目的是在D-半乳糖诱导的衰老动物模型中检测ASCs的抗衰老作用，并阐明其潜在的机制。材料与方法6周龄裸鼠皮下注射D-半乳糖，连续8周。治疗完成后两周，将小鼠随机接受皮下注射106个表达绿色荧光蛋白（GFP）的ASC、氨基胍（AG）或磷酸盐缓冲盐水（PBS）。对照小鼠不接受治疗。我们检查了组织组织学，并测定了衰老相关的分子标记物，如超氧化物歧化酶（SOD）和丙二醛（MDA）的活性。结果移植的ASCs可持续14 d，28 d后GFP信号消失。ASCs在我们的动物模型中抑制晚期糖基化终产物（AGE）水平，并增加SOD水平和降低MDA水平，所有这些都以与AG（AGE形成的抑制剂）相似的方式逆转衰老表型。此外，ASCs在体内释放血管生成因子，如血管内皮生长因子，表明皮肤营养作用。结论ASCs可能参与皮肤老化过程中的再生。此外，数据显示，ASC在小鼠衰老模型中通过糖化抑制、抗氧化和营养作用提供功能益处。
Introduction Glycation products accumulate during aging of slowly renewing tissue, including skin, and are suggested as an important mechanism underlying the skin aging process. Adipose-derived cells are widely used in the clinic to treat ischemic diseases and enhance wound healing. Interestingly, adipose-derived stem cells (ASCs) are also effective in anti-aging therapy, although the mechanism underlying their effects remains unknown. The purpose of the present study was to examine the anti-aging effect of ASCs in a D-galactose-induced aging animal model and to clarify the underlying mechanism. Materials and Methods Six-week-old nude mice were subcutaneously injected with D-gal daily for 8 weeks. Two weeks after completion of treatment, mice were randomized to receive subcutaneous injections of 106 green fluorescent protein (GFP)-expressing ASCs, aminoguanidine (AG) or phosphate-buffered saline (PBS). Control mice received no treatment. We examined tissue histology and determined the activity of senescence-associated molecular markers such as superoxide dismutase (SOD) and malondialdehyde (MDA). Results Transplanted ASCs were detectable for 14 days and their GFP signal disappeared at day 28 after injection. ASCs inhibited advanced glycation end product (AGE) levels in our animal model as well as increased the SOD level and decreased the MDA level, all of which act to reverse the aging phenotype in a similar way to AG, an inhibitor of AGE formation. Furthermore, ASCs released angiogenic factors in vivo such as vascular endothelial growth factor, suggesting a skin trophic effect. Conclusions These results demonstrate that ASCs may contribute to the regeneration of skin during aging. In addition, the data shows that ASCs provide a functional benefit by glycation suppression, antioxidation, and trophic effects in a mouse model of aging.
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