scholarly journals Low Intensity Pulsed Ultrasound Prevents Recurrent Ischemic Stroke in a Cerebral Ischemia/Reperfusion Injury Mouse Model via Brain-derived Neurotrophic Factor Induction

2019 ◽  
Vol 20 (20) ◽  
pp. 5169 ◽  
Author(s):  
Cheng-Tien Wu ◽  
Ting-Hua Yang ◽  
Man-Chih Chen ◽  
Yao-Pang Chung ◽  
Siao-Syun Guan ◽  
...  
Keyword(s):  
Mouse Model ◽  
Neurotrophic Factor ◽  
Recurrent Stroke ◽  
Brain Derived Neurotrophic Factor ◽  
Stroke Recurrence ◽  
Therapeutic Effects ◽  
Pulsed Ultrasound ◽  
Low Intensity Pulsed Ultrasound ◽  
Low Intensity ◽  
Therapeutic Benefits

The incidence of stroke recurrence is still higher despite the advanced progression of therapeutic treatment and medical technology. Low intensity pulsed ultrasound (LIPUS) has been demonstrated to possess therapeutic effects on neuronal diseases and stroke via brain-derived neurotrophic factor (BDNF) induction. In this study, we hypothesized that LIPUS treatment possessed therapeutic benefits for the improvement of stroke recurrence. Adult male C57BL/6J mice were subjected to a middle cerebral artery occlusion (MCAO) surgery and then followed to secondary MCAO surgery as a stroke recurrence occurred after nine days from the first MCAO. LIPUS was administered continuously for nine days before secondary MCAO. LIPUS treatment not only decreased the mortality but also significantly moderated neuronal function injury including neurological score, motor activity, and brain pathological score in the recurrent stroke mice. Furthermore, the administration of LIPUS attenuated the apoptotic neuronal cells and increased Bax/Bcl-2 protein expression ratio and accelerated the expression of BDNF in the brain of the recurrent stroke mice. Taken together, these results demonstrate for the first time that LIPUS treatment arouses the expression of BDNF and possesses a therapeutic benefit for the improvement of stroke recurrence in a mouse model. The neuroprotective potential of LIPUS may provide a useful strategy for the prevention of a recurrent stroke.

scholarly journals Low-intensity pulsed ultrasound improves behavioral functions and alleviates neuroinflammation in a rat model of Parkinson’s disease

2020 ◽  
Author(s):  
Feng-Yi Yang ◽  
Chen-Yu Sung ◽  
Pai-Kai Chiang ◽  
Che-Wen Tsai
Keyword(s):  
Rat Model ◽  
Neurotrophic Factors ◽  
Neurotrophic Factor ◽  
Tissue Injury ◽  
Substantia Nigra Pars Compacta ◽  
Dopamine Level ◽  
Pulsed Ultrasound ◽  
Low Intensity Pulsed Ultrasound ◽  
Low Intensity ◽  
The Brain

Abstract BackgroundParkinson’s disease (PD) is characterized by a reduction of dopamine level in the substantia nigra pars compacta (SNpc) and striatum of the brain. Low-intensity pulsed ultrasound (LIPUS) has been demonstrated recently as a non-invasive neuromodulation tool in a number of fields. LIPUS has also been reported to improve behavioral functions in PD animal models; however, the effect of LIPUS stimulation on the neurotrophic factors and neuroinflammation has not yet been addressed.MethodsPD rat model was built by injection of 6-hydroxydopamine (6-OHDA) in two sites in the right striatum. The levels of neurotrophic factors and lipocalin-2 (LCN2)-induced neuroinflammation were quantified using a western blot. Rotational test and cylinder test were conducted biweekly for eight weeks. The safety of LIPUS was assessed using Hematoxylin and Esosin (H&E) staining and Nissl staining.ResultsWhen the 6-OHDA+LIPUS and 6-OHDA groups were compared, the locomotor function of the 6-OHDA+LIPUS rats was significantly improved. After LIPUS stimulation, the number of neurons was remarkably increased in the striatum and SNpc of lesioned rats. Unilateral LIPUS stimulation did not increase brain-derived neurotrophic factor (BDNF) in the striatum and SNpc of lesioned rats. In contrast, unilateral LIPUS stimulation increased glial cell line-derived neurotrophic factor (GDNF) protein 1.98-fold unilaterally in the SNpc. Additionally, LCN2-induced neuroinflammation can be attenuated following LIPUS stimulation.ConclusionsOur data indicated that LIPUS stimulation increased GDNF and dopaminergic (DA) neuron density in the 6-OHDA-induced rat model of PD. Moreover, this technology attenuated proinflammatory mediators and reversed behavioral indicators of PD-associated motor dysfunction with no evidence of brain tissue injury. These results show that LIPUS stimulation may be a potential therapeutic tool against PD via enhancement of GDNF level and inhibition of inflammatory responses in the SNpc of the brain.

scholarly journals Protective effects of low-intensity pulsed ultrasound on aluminum overload-induced cerebral damage through epigenetic regulation of brain-derived neurotrophic factor expression

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Juan Li ◽  
Dong-dong Zhang ◽  
Chao-qing Wang ◽  
Miao Shi ◽  
Liang-liang Wang
Keyword(s):  
Histone Acetylation ◽  
Spatial Learning ◽  
Neurotrophic Factor ◽  
Spatial Learning And Memory ◽  
Cerebral Damage ◽  
Pulsed Ultrasound ◽  
Bdnf Expression ◽  
Low Intensity Pulsed Ultrasound ◽  
Low Intensity ◽  
Aluminium Exposure

Abstract In consideration of its noninvasive administration and endogenous stimulation property, the enhancement of brain-derived neurotrophic factor (BDNF) via low-intensity pulsed ultrasound (LIPUS) could be a novel strategy for aluminum (Al) overload-induced cerebral damage. LIPUS was pre-treated 7 days before concomitantly given with aluminum chloride (AlCl3) daily for a period of 42 days. Morris water maze and elevated plus maze were performed to analyze spatial learning and memory. Western Blot and immunoprecipitation were used to detect BDNF and histone acetylation of histone H3 lysine 9 (H3K9) and histone H4 lysine 12 (H4K12) in the hippocampus. Assay of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GSH-Px) indicated the extent of oxidative damages. Aluminium exposure in rats can cause attenuated spatial learning and memory, followed by up-regulated histone deacetylase 6 (HDAC6) expression, down-regulated H3K9 and H4K12 acetylation at the PIII and PIV promoter of BDNF, all of which will eventually inhibit BDNF expression. LIPUS can recover reduced cognitive function by restoring histone acetylation and BDNF expression, accompanied with increased SOD, GSH, and GSH-Px activity. LIPUS treatment might alleviate aluminium exposure-induced cognitive decline by acetylation regulation of BDNF expression and reducing oxidative stress in the hippocampus.

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