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低水平激光疗法通过激活 PI3K/Akt 信号通路诱导人脐静脉内皮细胞增殖、迁移和管腔形成。

Low-level laser therapy induces human umbilical vascular endothelial cell proliferation, migration and tube formation through activating the PI3K/Akt signaling pathway.

机构信息

Affiliated Eye Hospital of Nanchang University, Nanchang 330006, PR China.

Affiliated Eye Hospital of Nanchang University, Nanchang 330006, PR China.

出版信息

Microvasc Res. 2020 May;129:103959. doi: 10.1016/j.mvr.2019.103959. Epub 2019 Nov 14.

DOI:10.1016/j.mvr.2019.103959
PMID:31734375
Abstract

Low-level laser therapy (LLLT) has been recognized as a light therapy that may be used for tissue regeneration, inflammation reduction, and pain relief. We intended to evaluate the effects of LLLT on the proliferation, migration, and tube formation of HUVECs as well as their related mechanisms. HUVECs were exposed to laser irradiation under different laser parameters (irradiation dose, interval and power intensity) in order to choose the optimal parameters, which were determined by the increase in proliferation of HUVECs as follows: irradiation dose of 4.0 J/m, interval time of 12 h and 6 times in total. The HUVEC proliferation, migration, and tube formation, and levels of angiogenesis-related genes (HIF-1α, eNOS and VEGFA) were examined following LLLT. As suggested by the obtained data, LLLT (1.0, 2.0 and 4.0 J/m) increased the HUVEC proliferation, migration, and tube formation in dose-and time-dependent manner, accompanied with increases in the levels of HIF-1α, eNOS, and VEGFA. Furthermore, the regulatory mechanism regarding the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway was explored, phosphorylation levels of PI3K and Akt proteins were assessed by Western blot assay, which showed the enhancement of phosphorylation of PI3K, Akt, and mTOR by LLLT. The inhibitor for the PI3K/Akt axis was used to verify the involvement of PI3K/Akt signaling pathway. The obtained results suggested that the inhibition of the PI3K/Akt signaling pathway attenuated the effects of LLLT on proliferation, migration, and angiogenesis of HUVECs. In conclusion, LLLT promotes the proliferation, migration, and angiogenesis of HUVECs via activation of the PI3K/Akt signaling pathway.

摘要

低水平激光疗法(LLLT)已被认为是一种可能用于组织再生、炎症减轻和疼痛缓解的光疗方法。我们旨在评估 LLLT 对 HUVEC 增殖、迁移和管形成的影响及其相关机制。为了选择最佳参数,我们使 HUVEC 暴露于不同激光参数(辐照剂量、间隔时间和功率强度)下的激光照射下,这些参数是通过 HUVEC 增殖的增加来确定的,如下所示:辐照剂量为 4.0 J/m,间隔时间为 12 h,总共 6 次。在 LLLT 之后,检查了 HUVEC 增殖、迁移和管形成以及血管生成相关基因(HIF-1α、eNOS 和 VEGFA)的水平。根据获得的数据,LLLT(1.0、2.0 和 4.0 J/m)以剂量和时间依赖的方式增加了 HUVEC 的增殖、迁移和管形成,同时增加了 HIF-1α、eNOS 和 VEGFA 的水平。此外,还探讨了磷脂酰肌醇 3-激酶/蛋白激酶 B(PI3K/Akt)信号通路的调节机制,通过 Western blot 测定评估了 PI3K 和 Akt 蛋白的磷酸化水平,结果表明 LLLT 增强了 PI3K、Akt 和 mTOR 的磷酸化。使用 PI3K/Akt 轴抑制剂来验证 PI3K/Akt 信号通路的参与。结果表明,PI3K/Akt 信号通路的抑制减弱了 LLLT 对 HUVEC 增殖、迁移和血管生成的作用。总之,LLLT 通过激活 PI3K/Akt 信号通路促进 HUVEC 的增殖、迁移和血管生成。

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