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光生物调节对脂肪来源干细胞 AKT 表达的刺激作用可能介导了其体外伤口愈合潜能。

In Vitro Wound Healing Potential of Photobiomodulation Is Possibly Mediated by Its Stimulatory Effect on AKT Expression in Adipose-Derived Stem Cells.

机构信息

Laser Research Centre, University of Johannesburg, Johannesburg 2028, South Africa.

出版信息

Oxid Med Cell Longev. 2021 Jan 9;2021:6664627. doi: 10.1155/2021/6664627. eCollection 2021.

Abstract

Increasing evidence suggests that adipose-derived stem cells (ADSCs) serve as a therapeutic approach for wound healing. The aim of this study was to determine the effect of photobiomodulation (PBM) on antioxidant enzymes in ADSCs. Four ADSC cell models, namely, normal, wounded, diabetic, and diabetic wounded, were irradiated with 660 nm (fluence of 5 J/cm and power density of 11.2 mW/cm) or 830 nm (fluence of 5 J/cm and power density of 10.3 mW/cm). Nonirradiated cells served as controls. Cell morphology and wound migration were determined using light microscopy. Cell viability was determined by the trypan blue exclusion assay. The enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of antioxidants (superoxide dismutase (SOD), catalase (CAT), and heme oxygenase (HMOX1)). AKT activation and FOXO1 levels were determined by immunofluorescence and western blotting. The gaps (wound) in PBM-treated wounded and diabetic wounded cell models closed faster than the controls. PBM treatment significantly increased antioxidant levels in all cell models. This reflects that oxidative stress is reduced on the counterpart of increased antioxidant levels. This might be due to the activation of the AKT signaling pathway as evidenced by the increased AKT signals via western blotting and immunofluorescence. This data suggests that PBM promotes wound healing by increasing antioxidant levels by activating AKT signaling.

摘要

越来越多的证据表明脂肪来源的干细胞(ADSCs)可作为治疗伤口愈合的一种方法。本研究旨在确定光生物调节(PBM)对 ADSC 中抗氧化酶的影响。建立了四个 ADSC 细胞模型,分别为正常组、创伤组、糖尿病组和糖尿病创伤组,用 660nm(5J/cm 的辐照剂量和 11.2mW/cm 的功率密度)或 830nm(5J/cm 的辐照剂量和 10.3mW/cm 的功率密度)进行辐照。未辐照的细胞作为对照。通过相差显微镜观察细胞形态和伤口迁移。用台盼蓝排斥试验测定细胞活力。用酶联免疫吸附试验(ELISA)测定抗氧化剂(超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和血红素加氧酶 1(HMOX1))水平。通过免疫荧光和 Western blot 测定 AKT 激活和 FOXO1 水平。与对照组相比,PBM 处理的创伤和糖尿病创伤细胞模型中的间隙(伤口)愈合更快。PBM 处理显著增加了所有细胞模型中的抗氧化剂水平。这反映了在抗氧化剂水平增加的情况下,氧化应激减少。这可能是由于 AKT 信号通路的激活,这可以通过 Western blot 和免疫荧光检测到 AKT 信号的增加来证明。这些数据表明,PBM 通过激活 AKT 信号通路来增加抗氧化剂水平,从而促进伤口愈合。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/781e/7811432/90fc633eab00/OMCL2021-6664627.001.jpg

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