Treatment of experimentally induced transient cerebral ischemia with low energy laser inhibits nitric oxide synthase activity and up‐regulates the expression of transforming growth factor‐beta 1

Leung, Mason C.P.; Lo, Samuel Chun‐Lap; Siu, Flora K.W.; So, Kwok‐Fai

doi:10.1002/lsm.10096

Cited by 112 publications

(79 citation statements)

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“…7,8,15 Lapchak et al, 16 Oron et al, 17 and DeTaboada et al 18 have shown in 2 different animal models a positive impact of infrared laser therapy on the experimental, ischemic stroke treatment outcomes in New Zealand rabbits (rabbit small clot embolic stroke model [RSCEM]) and Sprague-Dawley rats (permanent middle cerebral artery occlusion). Lapchak has shown that laser treatment at 6 hours poststroke onset in RSCEM improved behavioral performance and produced a durable effect that was measurable 21 days after embolization.…”

mentioning

confidence: 99%

Infrared Laser Therapy for Ischemic Stroke: A New Treatment Strategy

Lampl

Zivin

Fisher

et al. 2007

Stroke

343

141

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Background and Purpose-The NeuroThera Effectiveness and Safety Trial-1 (NEST-1) study evaluated the safety and preliminary effectiveness of the NeuroThera Laser System in the ability to improve 90-day outcomes in ischemic stroke patients treated within 24 hours from stroke onset. The NeuroThera Laser System therapeutic approach involves use of infrared laser technology and has shown significant and sustained beneficial effects in animal models of ischemic stroke. Methods-This was a prospective, intention-to-treat, multicenter, international, double-blind, trial involving 120 ischemic stroke patients treated, randomized 2:1 ratio, with 79 patients in the active treatment group and 41 in the sham (placebo) control group. Only patients with baseline stroke severity measured by National Institutes of Health Stroke Scale (NIHSS) scores of 7 to 22 were included. Patients who received tissue plasminogen activator were excluded. Outcome measures were the patients' scores on the NIHSS, modified Rankin Scale (mRS), Barthel Index, and Glasgow Outcome Scale at 90 days after treatment. The primary outcome measure, prospectively identified, was successful treatment, documented by NIHSS. This was defined as a complete recovery at day 90 (NIHSS 0 to 1), or a decrease in NIHSS score of at least 9 points (day 90 versus baseline), and was tested as a binary measure (bNIH). Secondary outcome measures included mRS, Barthel Index, and Glasgow Outcome Scale. Primary statistical analyses were performed with the Cochran-Mantel-Haenszel rank test, stratified by baseline NIHSS score or by time to treatment for the bNIH and mRS. Logistic regression analyses were conducted to confirm the results. Results-Mean time to treatment was Ͼ16 hours (median time to treatment 18 hours for active and 17 hours for control).Time to treatment ranged from 2 to 24 hours. More patients (70%) in the active treatment group had successful outcomes than did controls (51%), as measured prospectively on the bNIH (Pϭ0.035 stratified by severity and time to treatment; Pϭ0.048 stratified only by severity). Similarly, more patients (59%) had successful outcomes than did controls (44%) as measured at 90 days as a binary mRS score of 0 to 2 (Pϭ0.034 stratified by severity and time to treatment; Pϭ0.043 stratified only by severity). Also, more patients in the active treatment group had successful outcomes than controls as measured by the change in mean NIHSS score from baseline to 90 days (Pϭ0.021 stratified by time to treatment) and the full mRS ("shift in Rankin") score (Pϭ0.020 stratified by severity and time to treatment; Pϭ0.026 stratified only by severity). The prevalence odds ratio for bNIH was 1.40 (95% CI, 1.01 to 1.93) and for binary mRS was 1.38 (95% CI, 1.03 to 1.83), controlling for baseline severity. Similar results held for the Barthel Index and Glasgow Outcome Scale. Mortality rates and serious adverse events (SAEs) did not differ significantly (8.9% and 25.3% for active 9.8% and 36.6% for control, respectively, for mortality and SAEs). Conclusion-The NE...

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mentioning

confidence: 99%

Infrared Laser Therapy for Ischemic Stroke: A New Treatment Strategy

Lampl

Zivin

Fisher

et al. 2007

Stroke

343

141

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“…Quando ocorre uma lesão tecidual, o processo de reparo é modulado pela atividade celular das células da resposta inflamatória e das células da borda da lesão e por uma rede de citocinas e de fatores de crescimento que influenciam a migração, a proliferação e a diferenciação celular para o local da lesão tecidual 26,27 . O TGF-β2 é uma citocina pró-inflamatória envolvida em processos fisiológicos e patológicos, incluindo remodelamento vascular (angiogênese e neogênese) e fibrose cutânea 26,[28][29][30] .…”

Section: Discussionunclassified

“…Os resultados sugeriram que a LLLT é um método útil e não invasivo para regular a intensidade da reação inflamatória, sendo instrumento importante na cicatrização de feridas cutâneas 6 . Estudo envolvendo tratamento com LLLT na isquemia cerebral induzida experimentalmente sugere que este tipo de terapia pode inibir a produção do NO e regular a expressão da citocina TGF-β2 que apresenta potencial anti--inflamatório além de induzir a proliferação fibroblástica, controlando o processo cicatricial 27 . Diversos pesquisadores também têm estudado o papel imunomodulador pró-inflamatório do NO através da elevação dos níveis de COX2 [14][15][16][17] .…”

Section: Discussionunclassified

Inibição da expressão de ciclooxigenase 2 em feridas cutâneas de camundongos NOD submetidos à terapia a laser de baixa intensidade

Rocha

Júnior²,

Aarestrup

et al. 2012

J. vasc. bras.

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ResumoContexto: A terapia a laser de baixa intensidade (LLLT) tem sido relatada como importante moduladora da cicatrização de feridas cutâneas aumentando a proliferação fibroblástica associada ao aumento da expressão da citocina fator transformador de crescimento-β2 (TGF-βB2). Objetivo: No presente estudo foram avaliados os efeitos da LLLT sobre a expressão da enzima ciclooxigenase 2 (COX2) no sítio do reparo tecidual utilizando o modelo experimental com camundongos diabéticos não obesos (NOD) para estudar a cicatrização de feridas cutâneas. Métodos: Foram utilizados 30 camundongos NOD, destes 14 ficaram diabéticos e foram divididos em dois grupos: o grupo I (n=7) foi submetido a um procedimento cirúrgico de feridas cutâneas e o grupo II (n=7) foi submetido a um procedimento cirúrgico de feridas cutâneas e tratados com LLLT. O grupo II foi submetido à LLLT nos seguintes parâmetros: 15 mW de potência, dose de 3,8 J/cm 2 e tempo de aplicação de 20 segundos. Após sete dias do ato cirúrgico e após aplicação do laser, os animais foram eutanasiados com sobredose de anestesia e amostras das feridas foram colhidas para posterior análise histopatológica, histomorfométrica e imuno-histoquímica. Resultados: A LLLT promoveu a inibição da expressão da COX2 em feridas cutâneas de camundongos diabéticos. Conclusão: Em conjunto, os resultados sugeriram que a LLLT é capaz de modular negativamente a expressão da enzima COX2 contribuindo para o controle da resposta inflamatória em feridas cutâneas de camundongos NOD.Palavras-chave: camundongos endogâmicos NOD; ciclooxigenase 2; terapia a laser de baixa intensidade. AbstractBackground: Low-level laser therapy (LLLT) has been reported to modulate the healing of wounds by inducing an increase in fibroblast number associated with increased expression of the cytokine transforming growth factor-β 2 (TGF-β 2 ). Objective: In the present study, the effect of LLLT on expression of COX2 at the site of tissue repair was evaluated, using an experimental model with non obese diabetic mice (NOD) to study cutaneous wound healing. Methods: Thirty NOD mice were used, of which 14 were diabetic and were divided into two groups: group I (n=7) underwent a surgical procedure of skin wounds and group II (n=7) underwent a surgical procedure of skin wounds and treated with LLLT. Group II was submitted to LLLT in the following parameters: 15 mW of power, dose of 3.8 J/cm 2 and exposure time of 20 seconds. Seven days after surgery and after laser application, animals were euthanized with an overdose of anesthesia and tissue samples were collected for subsequent histological analysis, histomorphometry and immunohistochemistry. Results: The LLLT has promoted the inhibition of COX2 expression in skin wounds in mice diabetic. Taken together the results suggest that LLLT modulate the expression of COX2 improved the control of inflammatory reaction in cutaneous wound lesions in NOD mice. Conclusion: Taken together, the results suggested that LLLT is able to negatively modulate the expression of COX2 enzyme contri...

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“…Although the specific mechanism remains unknown, laser-induced intracellular generation of reactive oxygen species probably involves energy transfer from PPIX and other photoacceptors present in the cell. In addition, several groups have described cellular functions mediated by nitric oxide (NO), which is upregulated by laser irradiation, as well as by inducible nitric oxide synthase (iNOS) [79,[81][82][83][84]. The mechanism of laser-induced control of cellular functions is believed to hinge on the regulation of photoacceptor activity and the intracellular levels of reactive oxygen species.…”

Section: Redox Pathwaysmentioning

confidence: 99%

Biological Function of Low Reactive Level Laser Therapy (LLLT)

Kubota¹,

Ishihara²

2017

Photomedicine - Advances in Clinical Practice

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Low reactive level laser therapy (LLLT) and photobiomodulation are mainly focused on the activation of intracellular or extracellular photoabsorbable molecule (chromophore) and the initiation of cellular signaling using low power lasers and lights. Over the past 40 decades, a number of basic and clinical researches were reported that the laser therapy had the potential to improve wound healing and reduce pain and inflammation. In recent years, the term "LLLT" has become widely recognized. In this review, the mechanisms of action of LLLT at a cellular level are described. Finally, our recent research results that LLLT enhanced the cells differentiation are also described.

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Treatment of experimentally induced transient cerebral ischemia with low energy laser inhibits nitric oxide synthase activity and up‐regulates the expression of transforming growth factor‐beta 1

Abstract: Low energy laser could suppress the activity of NOS and up-regulate the expression of TGF-beta1 after stroke in rats.

Cited by 112 publications

References 55 publications

Infrared Laser Therapy for Ischemic Stroke: A New Treatment Strategy

Infrared Laser Therapy for Ischemic Stroke: A New Treatment Strategy

Inibição da expressão de ciclooxigenase 2 em feridas cutâneas de camundongos NOD submetidos à terapia a laser de baixa intensidade

Biological Function of Low Reactive Level Laser Therapy (LLLT)

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