Produção Nacional
Revisado por pares
Dual Effect of low‐level laser therapy (LLLT) on the acute lung inflammation induced by intestinal ischemia and reperfusion: Action on anti‐ and pro‐inflammatory cytokines
2011; Wiley; Volume: 43; Issue: 5 Linguagem: Inglês
10.1002/lsm.21053
ISSN1096-9101
AutoresFlávia Mafra de Lima, Antônio Balbin Villaverde, Regiane Albertini, João Carlos Ferrari Corrêa, R.L.P. Carvalho, Egberto Munin, Ticiana Vasques Araújo, José Antônio Silva, Flávio Aimbire,
Tópico(s)Acupuncture Treatment Research Studies
ResumoIt is unknown if pro- and anti-inflammatory mediators in acute lung inflammation induced by intestinal ischemia and reperfusion (i-I/R) can be modulated by low-level laser therapy (LLLT).A controlled ex vivo study was developed in which rats were irradiated (660 nm, 30 mW, 0.08 cm² of spot size) on the skin over the right upper bronchus 1 hour post-mesenteric artery occlusion and euthanized 4 hours later. For pretreatment with anti-tumor necrosis factor (TNF) or IL-10 antibodies, the rats received either one of the agents 15 minutes before the beginning of reperfusion.Lung edema was measured by the Evans blue extravasation and pulmonary neutrophils influx was determined by myeloperoxidase (MPO) activity. Both TNF and IL-10 expression and protein in lung were evaluated by RT-PCR and ELISA, respectively.LLLT reduced the edema (80.1 ± 41.8 µg g⁻¹ dry weight), neutrophils influx (0.83 ± 0.02 × 10⁶ cells ml⁻¹), MPO activity (2.91 ± 0.60), and TNF (153.0 ± 21.0 pg mg⁻¹ tissue) in lung when compared with respective control groups. Surprisingly, the LLLT increased the IL-10 (0.65 ± 0.13) in lung from animals subjected to i-I/R. Moreover, LLLT (0.32 ± 0.07 pg ml⁻¹) reduced the TNF-α level in RPAECs when compared with i-I/R group. The presence of anti-TNF or IL-10 antibodies did not alter the LLLT effect on IL-10 (465.1 ± 21.0 pg mg⁻¹ tissue) or TNF (223.5 ± 21.0 pg mg⁻¹ tissue) in lung from animals submitted to i-I/R.The results indicate that the LLLT attenuates the i-I/R-induced acute lung inflammation which favor the IL-10 production and reduce TNF generation.
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