Porous Se@SiO(2) Nanoparticles Enhance Wound Healing by ROS-PI3K/Akt Pathway in Dermal Fibroblasts and Reduce Scar Formation.
Porous Se@SiO(2) Nanoparticles Enhance Wound Healing by ROS-PI3K/Akt Pathway in Dermal Fibroblasts and Reduce Scar Formation.
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DOI：
10.3389/fbioe.2022.852482
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发表时间：
2022
影响因子：
5.7
通讯作者：
Li XH
中科院分区：
文献类型：
--
作者：
Yang BY;Zhou ZY;Liu SY;Shi MJ;Liu XJ;Cheng TM;Deng GY;Tian Y;Song J;Li XH
以过度的细胞外基质沉积和异常的成纤维细胞稳态为特征的增生性瘢痕形成是皮肤伤口愈合的不良结果。瘢痕一旦形成，将取代局部皮肤的正常功能，并且很少有非侵入性的临床治疗方法可以治愈它。Se@SiO2纳米颗粒被合成以抑制氧化应激，其在伤口恢复期间诱导肌成纤维细胞的存在和活化。评价了Se@SiO2纳米粒的表征、抗氧化能力和生物安全性。建立全层切除创面模型，将创面分为3组。在特定处理后，使用苏木精和伊红染色以及Masson毛状体染色来评估再上皮化和胶原纤维的分布。我们的研究结果表明，Se@SiO2纳米粒子加速皮肤伤口愈合，抑制增生性瘢痕的形成，伴随着氧化应激抑制。此外，我们发现Se@SiO2 NPs通过激活PI 3 K/Akt通路并上调Akt的磷酸化而起作用。我们的研究结果提供了一种通过抑制过度氧化应激和通过PI 3 K/Akt通路激活来促进皮肤无瘢痕伤口愈合的新方法。
Hypertrophic scarring, which is characterized by excessive extracellular matrix deposition and abnormal fibroblast homeostasis, is an undesirable outcome of dermal wound healing. Once formed, the scar will replace the normal function of local skin, and there are few noninvasive clinical treatments that can cure it. Se@SiO2 nanoparticles were synthesized to suppress oxidative stress, which induced the presence and activation of myofibroblasts during wound recovery. The characterization, antioxidant capacity and biological safety of Se@SiO2 NPs were evaluated. A full-thickness excisional wound model was established, and the wounds were divided into three groups. The re-epithelization and distribution of collagen fibers were assessed using hematoxylin and eosin staining and Masson’s trichome staining after specific treatments. Our results revealed that the Se@SiO2 NPs accelerated dermal wound healing and suppressed the formation of hypertrophic scars, accompanied by oxidative stress inhibition. Moreover, we found that Se@SiO2 NPs worked by activating the PI3K/Akt pathway and upregulating the phosphorylation of Akt. The findings of our study provide a new method to promote dermal scar-free wound healing by suppressing excessive oxidative stress and through PI3K/Akt pathway activation.