Noise Induced Change Of Cochlea Stria Vascular And The Mechanism Of Its Regulation

Noise as part of environmental pollution abstracts people's mental, psychological and organ system. The most serious is the irreversible damage to the auditory system. The molecular mechanism of the injury of the stria vascular (SV) is to provide a more effective control for noise-induced hearing loss (NIHL).The later wall of the cochlea includes stria vascular (SV) and helical ligaments(SL).The blood-labyrinth barrier (BLB) at the SV plays an important role in maintaining EP, regulating the inner ear and body fluid balance. Noise-induced the BLB injury is one of the important factors of noise deafness. Previous studies have found that the BLB contains the endothelial cells (ECs) and basal membranes (BM), as well as pericytes (PCs) and perivascular macrophage-like melanocytes (PVM / Ms). PVM / Ms secreted pigment epithelium derived factor (PEDF), with anti-angiogenesis, anti-oxidation, protection of vascular permeability. Vascular endothelial growth factor A (VEGFA) has the effect of promoting angiogenesis and increasing vascular permeability. PEDF, VEGFA can regulate the expression of intercellular connexin, regulate BLB permeability. ZO-1, VE-Cadherin and Occludin are connexins in vascular BLB, which play an important role in maintaining BLB stability.In this study, we analyze and compare the distribution of PVM / Ms in SV at different time points before and after noise exposure. It was observed that PVM / Ms fluorescence staining was distributed in the later wall, the basement membrane and the spiral edge. It was found that the PVM / Ms fluorescence staining was decreased in the acute cochlea after noise exposure. The distribution of PVM / Ms fluorescence staining increased after 5 days of exposure, reached the peak at 5 days and returned to the pre-noise level after 14 days. PVM / Ms may promote vascular tissue repair by secreting PEDF, VEGFA, and increase the permeability of BLB.In order to study the effects of noise on PEDF, VEGFA and the effects of PEDF and VEGFA on connexin, we need more study. Western blot and real-time quantitative PCR(qPCR) were used to investigate the effect of PEDF and VEGF on the later wall connector protein and PEDF, VEGFA and its receptor VEGFR1, VEGFR2 were used to compare protein levels and mRNA levels. The expression of PEDF, VEGFA, VEGFR1, VEGFR2,VE-Cadherin and ZO-1 were down-regulated and Occludin was up-regulated in the acute phase after exposure. The expression of PEDF, ZO-1 and VE-Cadherin was up-regulated at NE7d, and reached the peak at NE14d. The expression of VEGFA1, VEGFR1 and VEGFR2 increased to the peak at the second day, and reached the peak atNE14d.Occlusion of noise in the NE to the NE2d down to the lowest value, followed by up-regulation.Through the study, it can be concluded that the acute radiation damage of PVM / Ms cells, foot retraction or cell surface antigen expression decreased, PEDF and connective protein expression decreased, increased vascular BLB permeability. The increase of PEDF expression promoted the expression of ZO-1 and VE-Cadherin, and promoted the repair of vascular BLB. Repair of early VEGFA expression increased, repair damaged microvascular endothelial cells, late due to antagonism of PEDF, VEGFA expression decreased. VEGFA had an inhibitory effect on ZO-1 and Occludin, and the expression of Occludin increased in the late stage of repair to further repair vascular BLB. PEDF,VEGFA and connexin have crossed the effect. According to our results, we conclude that the inhibitory effect of PEDF on ZO-1 is more obvious than that of VEGFA, and VEGFA has obvious inhibitory effect on Occludin. The study of noise-induced changes in PEDF,VEGFA and connexin, provides a new idea for the discovery of its molecular regulatory mechanism, providing a direction for further study of the mechanism of noise-induced vascular injury.