Sekhejane Palesa R, Houreld Nicolette N, Abrahamse Heidi
Laser Research Centre, Faculty of Health Sciences, University of Johannesburg, Doornfontein, South Africa.
Photomed Laser Surg. 2011 Aug;29(8):521-30. doi: 10.1089/pho.2010.2877. Epub 2011 Feb 19.
This study investigated the effect of low-intensity laser irradiation (LILI) on pro-inflammatory cytokines involved in wound healing processes in diabetes and hypoxia.
Diabetes is associated with impaired wound healing and a prolonged inflammatory phase. Pro-inflammatory cytokines such as interleukin (IL)-1β, tumor necrosis factor (TNF)-α and IL-6 are elevated in diabetes. LILI has been reported to accelerate wound healing and decrease inflammatory cytokines.
A human skin fibroblast cell line (WS1) was used in vitro. Cells were exposed to various insults, namely, wounding, and a diabetic or hypoxic environment. Experimental cells were exposed to an energy density of 5 J/cm(2) using a continuous wave 636-nm diode laser at an average power of 95 mW, an illuminated area of 9.05 cm(2), and an irradiance of 11 mW/cm(2) (irradiation time, 476 sec). The effect of laser irradiation on cytokine expression was examined at 1 or 24 h post-irradiation. Cellular morphology, viability, proliferation, and cytokine expression (IL-1β, IL-6, and TNF-α) were investigated. Translocation of nuclear factor-kappa B (NF-κB) was also determined.
There was a higher rate of migration in irradiated wounded cultures, and irradiated hypoxic cells showed an improvement in cellular morphology. All cell models showed an increase in proliferation. Normal wounded cells showed a decrease in apoptosis, TNF-α, and IL-1β. Diabetic wounded cells showed an increase in viability and a decrease in apoptosis and IL-1β, whereas hypoxic cells showed an increase in viability and IL-6, and a decrease in apoptosis and TNF-α. NF-κB was translocated into the nucleus post-irradiation.
Phototherapy resulted in hastened wound closure, increased proliferation, and normalization of cellular function. The decrease in the different pro-inflammatory cytokines and NF-κB translocation was model and time dependent. Overall, laser irradiation resulted in a reduction in inflammatory cytokines and directed cells into the cell survival pathway.
本研究调查了低强度激光照射（LILI）对糖尿病和缺氧状态下伤口愈合过程中促炎细胞因子的影响。
糖尿病与伤口愈合受损及炎症期延长有关。糖尿病患者体内促炎细胞因子如白细胞介素（IL）-1β、肿瘤坏死因子（TNF）-α和IL-6水平升高。据报道，低强度激光照射可加速伤口愈合并减少炎症细胞因子。
体外使用人皮肤成纤维细胞系（WS1）。细胞受到各种损伤，即创伤，以及糖尿病或缺氧环境。使用连续波636纳米二极管激光，平均功率95毫瓦，照射面积9.05平方厘米，辐照度11毫瓦/平方厘米（照射时间476秒），将实验细胞暴露于能量密度为5 J/cm²的激光下。在照射后1或24小时检查激光照射对细胞因子表达的影响。研究细胞形态、活力、增殖及细胞因子表达（IL-1β、IL-6和TNF-α）。还测定了核因子κB（NF-κB）的转位情况。
照射后的创伤培养物迁移率更高，照射后的缺氧细胞细胞形态有所改善。所有细胞模型的增殖均增加。正常创伤细胞的凋亡、TNF-α和IL-1β减少。糖尿病创伤细胞的活力增加，凋亡和IL-1β减少，而缺氧细胞的活力和IL-6增加，凋亡和TNF-α减少。照射后NF-κB转位至细胞核。
光疗可加速伤口闭合、增加增殖并使细胞功能正常化。不同促炎细胞因子的减少和NF-κB转位具有模型和时间依赖性。总体而言，激光照射可减少炎症细胞因子并引导细胞进入细胞存活途径。
