Laser Research Centre, Faculty of Health Sciences, University of Johannesburg, Johannesburg 2028, South Africa.
Oxid Med Cell Longev. 2021 Feb 13;2021:6667812. doi: 10.1155/2021/6667812. eCollection 2021.
Chemicals and signaling molecules released by injured cells at the beginning of wound healing prompt inflammation. In diabetes, prolonged inflammation is one of the probable causes for delayed wound healing. Increased levels of cyclooxygenase-2 (cox-2), interleukin-6 (IL-6), and tumour necrosis factor-alpha (TNF-) are associated with the inflammatory response and in diabetes, and increased levels of these contribute to chronic wounds that do not heal. Rising levels of cox-2, IL-6, and TNF- have also been associated with increased oxidative stress. Photobiomodulation (PBM) may impact wound healing processes by affecting the signaling pathways and molecules pertinent to tissue repair. In the present study, the effect of PBM (wavelength: 660 nm; energy density: 5 J/cm) on levels of cox-2, IL-6, and TNF- was determined in fibroblast cell culture models. Four WS1 models (normal, normal wounded, diabetic, and diabetic wounded) were irradiated at 660 nm, and the culture media was collected at 0, 24, and 48 h postirradiation. Cells that were not irradiated (0 J/cm) served as the controls. The following parameters were determined postirradiation: cell morphology using light microscopy, cell viability using the Trypan Blue exclusion assay, and levels of the inflammatory markers cox-2, IL-6, and TNF- were measured using ELISA. Cell migration increased in the wounded groups over the 48 h interval after PBM; viability improved postirradiation in the diabetic wounded groups at 0 and 24 h ( ≤ 0.05 and ≤ 0.01, respectively); levels of cox-2 decreased in normal and diabetic wounded groups at 0 h ( ≤ 0.001) and increased in the diabetic and diabetic wounded groups at 48 h postirradiation ( ≤ 0.05 and ≤ 0.01, respectively), while levels of IL-6 decreased in the normal ( ≤ 0.01), diabetic ( ≤ 0.05), and diabetic wounded ( ≤ 0.001) groups at 24 h and in the diabetic and diabetic wounded groups at 48 h ( ≤ 0.05) postirradiation. TNF- was decreased in the normal wounded groups ( ≤ 0.05) at 48 h. Through its effect on decreased IL-6 levels in diabetic cell models, PBM at 660 nm may be successful at decreasing oxidative stress; however, the present study also found an increase in cox-2 levels at 48 h postirradiation.
在伤口愈合的起始阶段,受伤细胞释放的化学物质和信号分子会引发炎症。在糖尿病中,长期的炎症是导致伤口愈合延迟的一个可能原因。环氧化酶-2(COX-2)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)水平升高与炎症反应有关,在糖尿病中,这些物质水平升高会导致慢性伤口无法愈合。COX-2、IL-6 和 TNF-α 水平升高也与氧化应激增加有关。光生物调节(PBM)可能通过影响与组织修复相关的信号通路和分子来影响伤口愈合过程。在本研究中,通过在成纤维细胞培养模型中测定 PBM(波长:660nm;能量密度:5J/cm)对 COX-2、IL-6 和 TNF-α 水平的影响,来评估 PBM 的效果。使用四个 WS1 模型(正常、正常受伤、糖尿病和糖尿病受伤)在 660nm 下进行辐照,并在辐照后 0、24 和 48 小时收集培养介质。未辐照(0J/cm)的细胞作为对照。辐照后测定以下参数:使用相差显微镜观察细胞形态,使用台盼蓝排除试验测定细胞活力,使用 ELISA 测定炎症标志物 COX-2、IL-6 和 TNF-α 的水平。PBM 后 48 小时内,受伤组的细胞迁移增加;糖尿病受伤组在辐照后 0 和 24 小时的活力提高(≤0.05 和 ≤0.01);正常和糖尿病受伤组在 0 小时 COX-2 水平降低(≤0.001),糖尿病和糖尿病受伤组在 48 小时后 COX-2 水平升高(≤0.05 和 ≤0.01),而正常(≤0.01)、糖尿病(≤0.05)和糖尿病受伤(≤0.001)组在 24 小时和糖尿病和糖尿病受伤组在 48 小时(≤0.05)后 IL-6 水平降低。48 小时后,正常受伤组 TNF-α 水平降低(≤0.05)。通过降低糖尿病细胞模型中 IL-6 水平的作用,660nm 的 PBM 可能成功降低氧化应激;然而,本研究还发现 48 小时后 COX-2 水平升高。