Aimbire F, Albertini R, Pacheco M T T, Castro-Faria-Neto H C, Leonardo P S L M, Iversen V V, Lopes-Martins R A B, Bjordal J M
Research Group of Fluorescence, IP&D UNIVAP R. Shishima Hifumi, São José dos Campos, São Paulo, Brazil.
Photomed Laser Surg. 2006 Feb;24(1):33-7. doi: 10.1089/pho.2006.24.33.
The aim of this study was to investigate if low-level laser therapy (LLLT) can modulate acute inflammation and tumor necrosis factor (TNFalpha) levels.
Drug therapy with TNFalpha-inhibitors has become standard treatment for rheumatoid arthritis, but it is unknown if LLLT can reduce or modulate TNFalpha levels in inflammatory disorders.
Two controlled animal studies were undertaken, with 35 male Wistar rats randomly divided into five groups each. Rabbit antiserum to ovalbumin was instilled intrabronchially in one of the lobes, followed by the intravenous injection of 10 mg of ovalbumin in 0.5 mL to induce acute lung injury. The first study served to define the time profile of TNFalpha activity for the first 4 h, while the second study compared three different LLLT doses to a control group and a chlorpromazine group at a timepoint where TNFalpha activity was increased. The rats in LLLT groups were irradiated within 5 min at the site of injury by a 650-nm Ga-Al-As laser.
There was a time-lag before TNFalpha activity increased after BSA injection. TNFalpha levels increased from < or =6.9 (95% confidence interval [CI], 5.6-8.2) units/mL in the first 3 h to 62.1 (95% CI, 60.8-63.4) units/mL (p < 0.001) at 4 h. An LLLT dose of 0.11 Joules administered with a power density of 31.3 mW/cm(2) in 42 sec significantly reduced TNFalpha level to 50.2 (95% CI, 49.4-51.0), p < 0.01 units/mL versus control. Chlorpromazine reduced TNFalpha level to 45.3 (95% CI, 44.0-46.6) units/mL, p < 0.001 versus control.
LLLT can reduce TNFalpha expression after acute immunocomplex lung injury in rats, but LLLT dose appears to be critical for reducing TNFalpha release.
本研究旨在调查低强度激光疗法（LLLT）是否能调节急性炎症和肿瘤坏死因子（TNFα）水平。
使用TNFα抑制剂进行药物治疗已成为类风湿性关节炎的标准治疗方法，但LLLT是否能降低或调节炎症性疾病中的TNFα水平尚不清楚。
进行了两项对照动物研究，将35只雄性Wistar大鼠随机分为五组。在其中一个肺叶内支气管内注入兔抗卵清蛋白抗血清，随后静脉注射0.5 mL含10 mg卵清蛋白的溶液以诱导急性肺损伤。第一项研究用于确定最初4小时内TNFα活性的时间变化情况，而第二项研究在TNFα活性增加的时间点，将三种不同剂量的LLLT与一个对照组和一个氯丙嗪组进行比较。LLLT组的大鼠在损伤部位于5分钟内用650纳米的镓铝砷激光进行照射。
注射牛血清白蛋白（BSA）后，TNFα活性增加存在时间延迟。TNFα水平在最初3小时从≤6.9（95%置信区间[CI]，5.6 - 8.2）单位/毫升增加到4小时时的62.1（95%CI，60.8 - 63.4）单位/毫升（p < 0.001）。以31.3毫瓦/平方厘米的功率密度在42秒内给予0.11焦耳的LLLT剂量可使TNFα水平显著降低至50.2（95%CI，49.4 - 51.0）单位/毫升，与对照组相比，p < 0.01。氯丙嗪可使TNFα水平降低至45.3（95%CI，44.0 - 46.6）单位/毫升，与对照组相比，p < 0.001。
LLLT可降低大鼠急性免疫复合物性肺损伤后的TNFα表达，但LLLT剂量对于降低TNFα释放似乎至关重要。
