论文部分内容阅读
目的研究噪声暴露对豚鼠耳蜗Bcl-2、Bax基因的表达及Bcl-2/Bax的影响,探讨噪声性听力损失(NIHL)的细胞凋亡机制。方法 36只SPF级健康雄性豚鼠随机分为对照组、95 d B、115 d B声压级(SPL)暴露组3组,每组12只,除对照组外分别予以95 d B、115 d B SPL的高斯白噪声暴露(28 d、6 h/d),暴露前1 d和暴露结束后d 7,分别进行听性脑干反应(ABR)测量、暴露结束后d 7进行耳蜗病理学检查和荧光实时定量逆转录-聚合酶链反应(RT-PCR)法分析耳蜗Bcl-2、Bax m RNA的相对表达水平。结果 3组间豚鼠永久性听阈位移(PTS)水平比较,差异有统计学意义(χ2=26.70,P<0.0001),95 d B、115 d B SPL组豚鼠耳蜗PTS水平分别为(12.50±2.50)、(27.50±2.50)(Md±(P75-P25));病理学显示噪声暴露组的豚鼠耳蜗毛细胞和螺旋神经节细胞出现明显损伤,高强度噪声暴露损伤程度比低强度暴露严重;Bcl-2、Bax m RNA表达水平和Bcl-2/Bax比值,在3组间均有统计学差异(χ2=20.35、22.89、23.48,P<0.0001);Bcl-2 m RNA表达水平随着噪声暴露强度的增加而下调;Bax m RNA表达水平在噪声暴露为115 d B SPL组显著上调;Bcl-2/Bax比值在95 d B和115 d B SPL两噪声暴露组中,均明显低于对照组,而且随着噪声暴露强度的增加而减少。结论 NIHL可诱导耳蜗细胞凋亡的发生,Bcl-2/Bax可作为评价耳蜗凋亡水平的指标。
Objective To investigate the effects of noise exposure on the expression of Bcl-2 and Bax gene and Bcl-2 / Bax in guinea pig cochlea and to explore the mechanism of apoptosis in noise-induced hearing loss (NIHL). Methods Thirty-six SPF healthy male guinea pigs were randomly divided into control group, 95 d B, 115 d B SPL exposure group, with 12 rats in each group. 95 d B, 115 d B SPL Gaussian white noise exposure (28 d, 6 h / d), 1 d before exposure and 7 d after exposure, respectively, for auditory brainstem response (ABR) measurements, d7 after cessation of the pathological examination and Real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to analyze the relative expression levels of Bcl-2 and Bax m RNA in cochleas. Results There was significant difference in permanent threshold shift (PTS) between the three groups (χ2 = 26.70, P <0.0001). The PTS levels in guinea pigs at 95 d B and 115 d BSPL were (12.50 ± 2.50) (P <0.05). (P <0.05). (P <0.05). (P <0.05). The pathological results showed that there were obvious damage in cochlear hair cells and spiral ganglion cells of guinea pig exposed to noise exposure, 2, Bax m RNA expression and Bcl-2 / Bax ratio in the three groups were statistically different (χ2 = 20.35,22.89,23.48, P <0.0001); Bcl-2 m RNA expression level with the noise exposure intensity Bcl-2 / Bax ratio was significantly lower than that of the control group at 95 d B and 115 d BSPL noise exposure groups, But also decreases as the noise exposure intensity increases. Conclusion NIHL can induce the apoptosis of cochlear cells. Bcl-2 / Bax may be used as an index to evaluate the apoptosis of cochlear.