Pre-conditioning with transcranial low-level light therapy reduces neuroinflammation and protects blood-brain barrier after focal cerebral ischemia in mice

• Published in: Restorative neurology and neuroscience Vol. 34; no. 2; pp. 201 - 214
• Main Authors: Lee, Hae In, Park, Jung Hwa, Park, Min Young, Kim, Nam Gyun, Park, Kyoung-Jun, Choi, Byung Tae, Shin, Yong-Ii, Shin, Hwa Kyoung
• Format: Journal Article
• Language: English
• Published: Netherlands 01.01.2016
• Subjects: Analysis of Variance; Animals; Blood-Brain Barrier - physiopathology; Brain Edema - etiology; Brain Edema - prevention & control; Brain Infarction - etiology; Brain Infarction - prevention & control; Brain Ischemia - complications; Brain Ischemia - etiology; Brain Ischemia - radiotherapy; Calcium-Binding Proteins - metabolism; Cytokines - genetics; Cytokines - metabolism; Encephalitis - etiology; Encephalitis - radiotherapy; Gene Expression Regulation - radiation effects; Intracranial Thrombosis - complications; Ischemic Preconditioning - methods; Leukocytes; Low-Level Light Therapy - methods; Male; Mice; Mice, Inbred C57BL; Microfilament Proteins - metabolism; Motor Activity; Neurologic Examination; Neutrophil Infiltration - physiology; blood-brain barrier; Low-level light therapy; focal cerebral ischemia; neuroinflammation
• ISSN: 0922-6028; 1878-3627
• DOI: 10.3233/RNN-150559

Transcranial low-level light therapy (LLLT) has gained interest as a non-invasive, inexpensive and safe method of modulating neurological and psychological functions in recent years. This study was designed to examine the preventive effects of LLLT via visible light source against cerebral ischemia at the behavioral, structural and neurochemical levels. The mice received LLLT twice a day for 2 days prior to photothrombotic cortical ischemia. LLLT significantly reduced infarct size and edema and improved neurological and motor function 24 h after ischemic injury. In addition, LLLT markedly inhibited Iba-1- and GFAP-positive cells, which was accompanied by a reduction in the expression of inflammatory mediators and inhibition of MAPK activation and NF-κB translocation in the ischemic cortex. Concomitantly, LLLT significantly attenuated leukocyte accumulation and infiltration into the infarct perifocal region. LLLT also prevented BBB disruption after ischemic events, as indicated by a reduction of Evans blue leakage and water content. These findings were corroborated by immunofluorescence staining of the tight junction-related proteins in the ischemic cortex in response to LLLT. Non-invasive intervention of LLLT in ischemic brain injury may provide a significant functional benefit with an underlying mechanism possibly being suppression of neuroinflammation and reduction of BBB disruption.