Low-level light emitting diode (LED) therapy suppresses inflammasome-mediated brain damage in experimental ischemic stroke.
Use of photostimulation including low-level light emitting diode (LED) therapy has broadened greatly in recent years because it is compact, portable, and easy to use. Here, the effects of photostimulation by LED (610 nm) therapy on ischemic brain damage was investigated in mice in which treatment started after a stroke in a clinically relevant setting. The mice underwent LED therapy (20 min) twice a day for 3 days, commencing at 4 hours post-ischemia. LED therapy group generated a significantly smaller infarct size and improvements in neurological function based on neurologic test score. LED therapy profoundly reduced neuroinflammatory responses including neutrophil infiltration and microglia activation in the ischemic cortex. LED therapy also decreased cell death and attenuated the NLRP3 inflammasome, in accordance with down-regulation of pro-inflammatory cytokines IL-1β and IL-18 in the ischemic brain. Moreover, the mice with post-ischemic LED therapy showed suppressed TLR-2 levels, MAPK signaling and NF-kB activation. These findings suggest that by suppressing the inflammasome, LED therapy can attenuate neuroinflammatory responses and tissue damage following ischemic stroke. Therapeutic interventions targeting the inflammasome via photostimulation with LED may be a novel approach to ameliorate brain injury following ischemic stroke. Effect of post-ischemic low-level light emitting diode therapy (LED-T) on infarct reduction was mediated by inflammasome suppression.
Department of Rehabilitation Medicine, School of Medicine, Pusan National University, Yangsan, Gyeongnam 626-870, Republic of Korea.
Hae In
HI
Lee
Korean Medical Science Research Center for Healthy-Aging, Pusan National University, Yangsan, Gyeongnam 626-870, Republic of Korea.|Department of Korean Medical Science, School of Korean Medicine, Pusan National University, Yangsan, Gyeongnam 626-870, Republic of Korea.
Sae-Won
SW
Lee
Medical Research Center of Color Seven, Seoul 137-867, Republic of Korea.
Nam Gyun
NG
Kim
Medical Research Center of Color Seven, Seoul 137-867, Republic of Korea.
Kyoung-Jun
KJ
Park
Korean Medical Science Research Center for Healthy-Aging, Pusan National University, Yangsan, Gyeongnam 626-870, Republic of Korea.|Department of Korean Medical Science, School of Korean Medicine, Pusan National University, Yangsan, Gyeongnam 626-870, Republic of Korea.|Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University, Yangsan, Gyeongnam 626-870, Republic of Korea.
Byung Tae
BT
Choi
Department of Rehabilitation Medicine, School of Medicine, Pusan National University, Yangsan, Gyeongnam 626-870, Republic of Korea.|Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan, Gyeongnam 626-770, Republic of Korea.
Yong-Il
YI
Shin
Korean Medical Science Research Center for Healthy-Aging, Pusan National University, Yangsan, Gyeongnam 626-870, Republic of Korea.|Department of Korean Medical Science, School of Korean Medicine, Pusan National University, Yangsan, Gyeongnam 626-870, Republic of Korea.|Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University, Yangsan, Gyeongnam 626-870, Republic of Korea.
Hwa Kyoung
HK
Shin
D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000473:pathology / Q000528:radiation effects*; D002545:Brain Ischemia / Q000150:complications*; D016923:Cell Death / Q000528:radiation effects; D004195:Disease Models, Animal; D058847:Inflammasomes / Q000378:metabolism*; D028022:Low-Level Light Therapy; D051379:Mice; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D020521:Stroke / Q000150:complications* / Q000378:metabolism / Q000532:radiotherapy*; D051195:Toll-Like Receptor 2 / Q000378:metabolism
D058847:Inflammasomes; C493486:Tlr2 protein, mouse; D051195:Toll-Like Receptor 2; D020928:Mitogen-Activated Protein Kinases
Focal cerebral ischemia; NLRP3; TLR2; neuroprotection; photostimulation 