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噪声性听力损失与耳蜗毛细胞Caspase-3表达的相关性分析 被引量:1

The correlation analysis between noise-induced hearing loss and the expression of Caspase-3 in the hair cells
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摘要 目的探讨不同程度的噪声性听力损失(NIHL)豚鼠耳蜗毛细胞Caspase-3表达水平与永久性听阈位移(PTS)水平的关系,分析毛细胞的噪声损伤机制。方法 SPF级雄性豚鼠60只随机分为对照组和85、95、105、115dB SPL暴露组。暴露组分别给予上述强度的高斯白噪声,每天6h,连续28d。暴露前1d和暴露结束后第7天进行听性脑干反应(ABR)测量,以及耳蜗病理学检查。免疫组化法分析耳蜗毛细胞的Caspase-3表达水平。结果各组间豚鼠平均PTS水平变化均有统计学意义(F=327.04,P<0.01),在噪声暴露强的组PTS水平增加明显。各组豚鼠毛细胞的Caspase-3吸光度(A)值差异有统计学意义(F=37.9,P<0.01),115dB噪声暴露组明显高于其他暴露组(P<0.01),105、95、85dB噪声暴露组之间比较,差异无统计学意义(P>0.05),但明显高于对照组(P<0.01)。病理学观察发现,各噪声暴露组均出现毛细胞的损伤,大于105dB暴露组出现毛细胞坏死现象。结论 NIHL可诱发耳蜗毛细胞的凋亡和坏死,坏死的发生早于凋亡的发生。 Objective To explore the relationship between the expression level of Caspase-3 in cochlea hair cells of guinea pig with different levels of noise hearing loss(NIHL)and the level of Permanent displacement of auditory threshold(PTS),and to analyze mechanisms of noise damage in hair cells.Methods 60 SPF male guinea pigs were randomly divided into control group and 4exposed groups including 85,95,105,115 dB SPL.Four exposed groups were exposed to Gaussian white noise for 6ha day in 28 d.The auditory brainstem response were measured at one day before exposure and 7days after exposure.Cochlear pathology examination and immunohistochemistry were used to analyze the expression of caspase-3in hair cells.Results There was significant difference among the groups(F=327.04,P〈0.01),increased level of PTS were observed in exposed group with higher intensity noise.The expression of Caspase-3 in guinea pig hair cells had significant difference in the groups(F=37.9,P〈0.01).exposed group with 115 dB SPL had the highest level of Caspase-3 (P〈0.01),other exposed groups showed no significant difference(P〉0.05),but they were higher than the control one's.The pathological observation found hair cells damage in the exposed groups,necrosis of hair cells were found in the exposed groups with 105 and 115dB SPL.Conclusions NIHL can induce the apoptosis and necrosis,and necrosis occurred earlier than the occurrence of apoptosis.
作者 夏源 张敏 杨翠婵 王军义 XIA Yuan ZHANG Min YANG Cui-chan WANG Jun-yi(School of Public Health GuangDong Pharmaceutical University, Guangzhou 510310 China)
出处 《工业卫生与职业病》 CAS 2017年第2期85-88,共4页 Industrial Health and Occupational Diseases
基金 基金项目 广东省职业病防治重点实验室(2012A061400007-01)
关键词 噪声性听力损失 毛细胞 坏死 凋亡 Noise induced hearing loss Hair cell Necrosis Apoptosis
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  • 1杨光华,温秀兰,王宝珍,钱锦康.模拟失重(HDT—30°)和噪声复合因素对大鼠神经-内分泌-免疫功能的影响[J].空间科学学报,1994,14(3):210-213. 被引量:13
  • 2贾佳,杨振军,周鹏,徐运.雌激素抑制Fas相关死亡结构域蛋白保护缺血性脑损伤[J].医学研究生学报,2007,20(3):249-252. 被引量:8
  • 3Jackson TC, Rani A, Kumar A, Foster TC. Regional hippocampal differences in AKT survival signaling across the lifespan: implica- tions for CA1 vulnerability with aging. Cell Death Differ 2009, 16: 439-448.
  • 4Nie K, Yu JC, Fu Y, Cheng HY, Chen FY, Qu Y, et al. Age-related decrease in constructive activation of Akt/PKB in SAMP10 hip- pocampus. Biochem Biophys Res Commun 2009, 378:103-107.
  • 5Andjelkovic M, Alessi DR, Meier R, Fernandez A, Lamb NJ, Frech M, et al. Role oftranslocation in the activation and function of pro- tein kinase B. J Biol Chem 1997, 272: 31515-31524.
  • 6Bellacosa A, Chan TO, Ahmed NN, Datta K, Malstrom S, Stokoe D, et al. Akt activation by growth factors is a multiple-step process: the role of the PH domain. Oncogene 1998, 17: 313-325.
  • 7Song G, Ouyang G, Bao S. The activation of Akt/PKB signaling pathway and cell survival. J Cell Mol Med 2005, 9: 59-71.
  • 8Pastor MD, Garcia-Yebenes I, Fradejas N, P6rez-Ortiz JM, Mora- Lee S, Tranque P, et al. mTOR/S6 kinase pathway contributes to astrocyte survival during ischemia. J Biol Chem 2009, 284(33): 22067-22078.
  • 9Condorelli F, Salomoni P, Cotteret S, Cesi V, Srinivasula SM, AI- nemri ES, et al. Caspase cleavage enhances the apoptosis-inducing effects of BAD. Mol Cell Biol 2001, 21: 3025-3036.
  • 10Cardone MH, Roy N, Stennicke HR, Salvesen GS, Franke TF, Stanbridge E, et al. Regulation of cell death protease caspase-9 by phosphorylation. Science 1998, 282:1318-1321.

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