Preliminary evidence suggest that low intensity pulsed ultrasound (LIPUS) has neuroprotective effects on ischemic stroke, d epression and other conditions leading to neuronal cell death (e.g., Pa rkinson's disease). The purpose of this study was to investigate the n europrotective effects of LIPUS in epileptic mice. METHODS: Mice we re made epileptic through Kainic Acid (KA) administration and then stimulated with LIPUS. The neuroprotective effect of ultrasound was evaluated by observing the latency, anxiety-like behavior, and levels of proteins related to inflammation, apoptosis, or signaling pathways. The safety of LIPUS was assessed by hematoxylin and eosin (H&E) and Nissl stainings. RESULTS: LIPUS prolonged the latency (Sham = 6. 00 ± 0.26 days; 1 kHz PRF = 7.00 ± 0.31 days), improved the anxiety -like behavior, and inhibited the expression of inflammatory factors and apoptosis-related proteins. Additionally, H&E and Nissl staining results confirmed that LIPUS did not damage the brain. CONCLUSION: These findings suggest that LIPUS has neuroprotective effects in mic e with KA-induced epilepsy. SIGNIFICANCE: LIPUS may offer a new th erapeutic approach to epilepsy.
Preliminary evidence suggest that low intensity pulsed ultrasound (LIPUS) has neuroprotective effects on ischemic stroke, d epression and other conditions leading to neuronal cell death (e.g., Pa rkinson's disease). The purpose of this study was to investigate the n europrotective effects of LIPUS in epilepticmice. METHODS:Mice we re made epileptic through Kainic Acid (KA) administration and then stimulated with LIPUS. The neuroprotective effect of ultrasound was evaluated by observing the latency, anxiety-like behavior, and levels of proteins related to inflammation, apoptosis, or signaling pathways. The safety of LIPUS was assessed by hematoxylin and eosin (H&E) and Nissl stainings. RESULTS: LIPUS prolonged the latency (Sham = 6. 00 ± 0.26 days; 1 kHz PRF = 7.00 ± 0.31 days), improved the anxiety -like behavior, and inhibited the expression of inflammatory factors and apoptosis-related proteins. Additionally, H&E and Nissl staining results confirmed that LIPUS did not damage the brain. CONCLUSION: These findings suggest that LIPUS has neuroprotective effects in mic e with KA-induced epilepsy. SIGNIFICANCE: LIPUS may offer a new th erapeutic approach to epilepsy.