کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5738052 | 1615037 | 2018 | 7 صفحه PDF | دانلود رایگان |
- The opening of BBB caused by low-frequency but high-intensity noise exposure is discovered firstly.
- Noise induced BBB impairment is related with down-regulation of zo-1 and occludin.
- The activation of CysLT1R could regulate noise-induced tight junction defects.
ObjectivesVibroacousitic disease (VAD) is caused by excessive exposure to low-frequency but high-intensity noise. The integrity of the brain blood barrier (BBB) is essential for the brain. The study aimed to investigate the effect of noise exposure on the BBB.MethodsHealthy male Bama swine were exposed to 50, 70, 100, and 120Â Hz, 140Â dB noise for 30Â min. After exposure, CT brain imaging and ex vivo fluorescent imaging of parenchymal EB leakage were performed (each group consisted of NÂ =Â 3 swine). The human cerebral microvascular endothelial cells were exposed to 70Â Hz, 140Â dB noise for 5Â min.ResultsThe BBB permeability assay showed that 50, 70, and 100Â Hz with 140Â dB noise exposure accelerated BBB permeability, and the BBB opening at 70Â Hz was most serious and reversible. Additionally, CT images demonstrated that the noise-induced opening of the BBB caused no intracerebral hemorrhage. This noise-induced BBB opening was related to the downregulation of zo-1 and occludin. Finally, cysteinyl leukotriene receptor 1 (CysLT1 receptor) was found to regulate noise-induced tight junction defects in vitro.ConclusionsIn conclusion, noise exposure accelerates the formation of a high-permeability BBB with leaky tight junctions through a CysLT1-mediated mechanism, which warrants additional research.
Journal: Neuroscience Letters - Volume 662, 1 January 2018, Pages 122-128