Acute Noise Causes Down-Regulation of ECM Protein Expression in Guinea Pig Cochlea.

Proteomics technology reveals the marker proteins, potential pathogenesis, and intervention targets after noise-induced hearing loss. To study the differences in cochlea protein expression before and after noise exposure using proteomics to reveal the pathological mechanism of noise-induced hearing loss (NIHL). A guinea pig NIHL model was established to test the ABR thresholds before and after noise exposure. The proteomics technology was used to study the mechanism of differential protein expression in the cochlea by noise stimulation. The average hearing threshold of guinea pigs on the first day after noise exposure was 57.00 ± 6.78 dB Sound pressure level (SPL); the average hearing threshold on the seventh day after noise exposure was 45.83 ± 6.07 dB SPL. The proteomics technology identified 3122 different inner ear proteins, of which six proteins related to the hearing were down-regulation: Tenascin C, Collagen Type XI alpha two chains, Collagen Type II alpha one chain, Thrombospondin 2, Collagen Type XI alpha one chain and Ribosomal protein L38, and are enriched in protein absorption, focal adhesion, and extracellular matrix receptor pathways. Impulse noise can affect the expression of differential proteins through focal adhesion pathways. This data can provide an experimental basis for the research on the prevention and treatment of NIHL.

[Effects of tetramethylpyrazine on expression of vascular endothelial growth factor and hypoxia-induced factor-1alpha by rat peritoneal macrophages].

OBJECTIVE: To investigate the effects of tetramethylpyrazine on lipopolysaccharides (LPS)-induced expression of vascular endothelial growth factor (VEGF) and hypoxia-induced factor-1alpha (HIF-1alpha) in macrophages. METHOD: Rat peritoneal macrophages were treated with LPS, and at the same time given different doses of tetramethylpyrazine. The secreation of VEGF was determined by ELISA test, and MTT assay was used to examine cells proliferation. Western blot assay was used to examine the expression of HIF-1alpha. RESULT: 100 microg x mL(-1) and 10 microg x mL(-1) tetramethylpyrazine decreased the secretion of VEGF and also inhibited the expression of HIF-1alpha by LPS-induced macrophages. But these doses of tetramethylpyrazine had no effect on the cells proliferation. CONCLUSION: Tetramethylpyrazine could inhibit the secretion of VEGF by LPS-induced macrophages, and the mechanism must be associated with inhibiting the expression of HIF-1alpha. The inhibition effect was not due to inhibition of the proliferation of macrophages.