Dos Anjos Lúcia Mara Januário, da Fonseca Adenilson de Souza, Gameiro Jacy, de Paoli Flávia
Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Juiz de Fora, Rua José Lourenço Kelmer, s/n-Campus Universitário, São Pedro, Juiz de Fora, Minas Gerais, 36036900, Brazil.
Departamento de Biofísica e Biometria, Instituto de Biologia Roberto Alcântara Gomes, Universidade do Estado do Rio de Janeiro, Rua São Francisco Xavier, 524, Maracanã, Rio de Janeiro, 20550900, Brazil.
Lasers Med Sci. 2017 Jul;32(5):975-983. doi: 10.1007/s10103-017-2196-8. Epub 2017 Apr 5.
Anti-inflammatory property of low-level laser therapy (LLLT) has been widely described in literature, although action mechanisms are not always clarified. Thus, this study aimed to evaluate apoptosis mechanisms in the LLLT anti-inflammatory effects on the arthritis experimental model in vivo at two different energy densities (3 and 30 Jcm). Arthritis was induced in mice by zymosan solution, animals were distributed into five groups, and morphological analysis, immunocytochemistry and gene expressions for apoptotic proteins were performed. Data showed an anti-inflammatory effect, DNA fragmentation in polymorphonuclear (PMN) cells and alteration in gene expression of proteins related to apoptosis pathways after LLLT. p53 gene expression increased at both energy densities, Bcl2 gene expression increased at 3 Jcm, and Bcl2 tissue expression decreased at 30 Jcm. In addition, apoptosis was restricted to PMN cells. Results suggest that apoptosis in PMN cells comprise part of LLLT anti-inflammatory mechanisms by disbalance promotion between expression of pro-apoptotic (Bax and p53) and anti-apoptotic (Bcl-2) proteins, with pro-apoptotic gene expression selectively in PMN cells.
低强度激光疗法(LLLT)的抗炎特性在文献中已有广泛描述,尽管其作用机制并不总是很清楚。因此,本研究旨在评估在两种不同能量密度(3和30 J/cm)下,LLLT对体内关节炎实验模型的抗炎作用中的细胞凋亡机制。通过酵母聚糖溶液诱导小鼠患关节炎,将动物分为五组,并进行形态学分析、免疫细胞化学和凋亡蛋白的基因表达检测。数据显示,LLLT后具有抗炎作用、多形核(PMN)细胞中的DNA片段化以及与凋亡途径相关的蛋白质基因表达改变。在两种能量密度下p53基因表达均增加,在3 J/cm时Bcl2基因表达增加,而在30 J/cm时Bcl2组织表达降低。此外,细胞凋亡仅限于PMN细胞。结果表明,PMN细胞中的细胞凋亡通过促凋亡蛋白(Bax和p53)与抗凋亡蛋白(Bcl-2)表达之间的失衡促进,且促凋亡基因在PMN细胞中选择性表达,从而构成了LLLT抗炎机制的一部分。