Objectives: Transcranial low-level light therapy (LLLT) has gained interest as a non-invasive, inexpensive and safe method of modulating neurological and psychological functions or inducing neurotherapeutic effects in recent years. Integrated responses in neurovascular unit, comprising neuronal, gli...
Objectives: Transcranial low-level light therapy (LLLT) has gained interest as a non-invasive, inexpensive and safe method of modulating neurological and psychological functions or inducing neurotherapeutic effects in recent years. Integrated responses in neurovascular unit, comprising neuronal, glial and vascular compartment all contribute to the development of ischemic brain injury. Therefore, this study was designed to examine the preventive and protective effects of LLLT on neuronal cell death, neuroinflammation and blood-brain barrier (BBB) dysfunction induced by focal cerebral ischemic brain injury. Methods: LLLT was applied transcranially via the exposed skull by placing the LLLT device onto the skin at two locations on the head (the right midpoint of the parietal bone and the posterior midline of the seventh cervical vertebra). The mice received LLLT (20 min) twice a day for 2 days before or after the ischemic event. Focal cerebral ischemia was induced in C57BL/6J mice using a photothrombotic cortical ischemia model. The effects of LLLT were evaluated at behavioral, structural and neurochemical levels 24 h or 48 h after ischemic brain injury. Results: LLLT treatment prior to ischemic insult significantly reduced infarct size and edema and improved neurological and motor function. Staining of Iba-1 and GFAP showed that LLLT markedly inhibited microglia and astrocyte activation in the ischemic cortex, which was accompanied by a reduction in the expression and production of iNOS, COX-2, TLR-2, proinflammatory cytokines (TNF-α and IL-1β) and chemokines (CCL2 and CXCL10). Moreover, LLLT exhibited anti-inflammatory properties via downregulation of MAPK pathways and NF-κB translocation. In addition, LLLT profoundly reduced the number of myeloperoxidase (MPO)-positive cells and MPO protein levels in the ischemic cortex. LLLT also prevented BBB disruption after ischemic brain injury, as indicated by a reduction of Evans blue extravasation and water content. These findings were corroborated by reductions in ZO-1, occludin, claudin-5 expression in the ischemic cortex in response to LLLT. Furthermore, LLLT obviously inhibited the neuronal cell death after stroke. Therefore, noninvasive exposure of LLLT to the brain before cerebral ischemia significantly prevented the neuroinflammation, BBB damage and neuronal cell death. Finally, the neuroprotective efficacy was determined if the treatment started after ischemic brain injury in a clinically relevant setting. LLLT treatment after ischemic insult significantly decreased infarct volume and improved neurological deficits as well as attenuated neuronal cell death. Conclusion: Noninvasive intervention of LLLT in focal cerebral ischemic injury may provide a better modality via the management of neurovascular unit in ischemic stroke.
Objectives: Transcranial low-level light therapy (LLLT) has gained interest as a non-invasive, inexpensive and safe method of modulating neurological and psychological functions or inducing neurotherapeutic effects in recent years. Integrated responses in neurovascular unit, comprising neuronal, glial and vascular compartment all contribute to the development of ischemic brain injury. Therefore, this study was designed to examine the preventive and protective effects of LLLT on neuronal cell death, neuroinflammation and blood-brain barrier (BBB) dysfunction induced by focal cerebral ischemic brain injury. Methods: LLLT was applied transcranially via the exposed skull by placing the LLLT device onto the skin at two locations on the head (the right midpoint of the parietal bone and the posterior midline of the seventh cervical vertebra). The mice received LLLT (20 min) twice a day for 2 days before or after the ischemic event. Focal cerebral ischemia was induced in C57BL/6J mice using a photothrombotic cortical ischemia model. The effects of LLLT were evaluated at behavioral, structural and neurochemical levels 24 h or 48 h after ischemic brain injury. Results: LLLT treatment prior to ischemic insult significantly reduced infarct size and edema and improved neurological and motor function. Staining of Iba-1 and GFAP showed that LLLT markedly inhibited microglia and astrocyte activation in the ischemic cortex, which was accompanied by a reduction in the expression and production of iNOS, COX-2, TLR-2, proinflammatory cytokines (TNF-α and IL-1β) and chemokines (CCL2 and CXCL10). Moreover, LLLT exhibited anti-inflammatory properties via downregulation of MAPK pathways and NF-κB translocation. In addition, LLLT profoundly reduced the number of myeloperoxidase (MPO)-positive cells and MPO protein levels in the ischemic cortex. LLLT also prevented BBB disruption after ischemic brain injury, as indicated by a reduction of Evans blue extravasation and water content. These findings were corroborated by reductions in ZO-1, occludin, claudin-5 expression in the ischemic cortex in response to LLLT. Furthermore, LLLT obviously inhibited the neuronal cell death after stroke. Therefore, noninvasive exposure of LLLT to the brain before cerebral ischemia significantly prevented the neuroinflammation, BBB damage and neuronal cell death. Finally, the neuroprotective efficacy was determined if the treatment started after ischemic brain injury in a clinically relevant setting. LLLT treatment after ischemic insult significantly decreased infarct volume and improved neurological deficits as well as attenuated neuronal cell death. Conclusion: Noninvasive intervention of LLLT in focal cerebral ischemic injury may provide a better modality via the management of neurovascular unit in ischemic stroke.
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