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顺铂导致螺旋神经节细胞凋亡中pp38MAPK和pERK信号蛋白的作用 被引量:1

Detection of pp38MAPK and pERK in SGCs after the Application of Cisplatin(Cddp)and Apoptosis of Cisplatin(Cddp)-Induced SGCs
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摘要 目的初步探讨丝裂素活化蛋白激酶(mitogen-activated proteins kinase,MAPK)信号转导通路中磷酸化p38MAPK蛋白(pp38MAPK)和磷酸化ERK蛋白(pERK)在顺铂耳毒性中的作用。方法选取20只健康豚鼠随机分为两组,每组10只,实验组腹腔注射顺铂4mg·kg-1·d-1,连续4天,对照组腹腔注射等量生理盐水。最后一次给药后24小时内处死动物、取材,HE染色后光镜下观察内耳螺旋神经节细胞形态学变化;透射电镜下观察螺旋神经节细胞的凋亡情况;免疫组化染色法观察螺旋神经节细胞pp38MAPK和pERK蛋白的表达。结果实验组豚鼠螺旋神经节细胞数目减少、体积减小,排列散乱,出现凋亡改变,而对照组螺旋神经节细胞无明显凋亡改变。pp38MAPK主要分布在螺旋神经节细胞胞浆,对照组表达较弱(平均光密度值为0.12±0.04),实验组表达增强(平均光密度值为0.24±0.07),两组差异有统计学意义(t=4.581,P<0.05)。pERK在螺旋神经节细胞的胞浆有表达,对照组的平均光密度值为0.27±0.08,实验组的平均光密度值为0.25±0.08,两组差异无统计学意义(t=-0.673,P>0.05)。结论 pp38MAPK可能参与了顺铂导致豚鼠螺旋神经节细胞的凋亡。 Objective To investigate the expression of pp38MAPK and pERK proteins in guinea pig cochlea injuried by cisplatin(Cddp). Methods Twenty guinea pigs were divided into two groups (10 guinea pigs in each groups) :cisplatin group and control group (NaCl 0.9% NS). In the cisplatin group, 4 mg · kg-1 · d-1 of cisplatin dissolved in 0.9 % saline(NS) was injected intraperitoneally, while in the control group, only physiological saline was injected. All animals were sacrificed four days after the injection and the temporal bones were removed and then used for immunohistochemical examinations,or transmission electron microscopy examinations. Results The resuts of electron microscopy showed the special morphological changes consistent with the features of cell apoptosis in some spiral ganglion cells after 4 dayg cisplatin treatment, whereas almost negative results were obtained in the sa- line control animals. Pp38MAPK faint staining was found in spiral ganglion cells in control group(MOD= 0.12± 0. 04), and in the eddp group, the expression of pp38MAPK had a significant increase following 4 days' cisplatin administration, especially in cytoplasm of spiral ganglion ceil (MOD = 0. 24 ± 0.07, t = 4. 581, P 〈 0. 05). PERK showed very faint staining in spiral ganglion cells, and no specific immunolabelling in control group(MOD=0. 27± 0.08), while in cddp group, pERK staining was very faint(MOD=0.25±0.08,t=-0. 673,P〉0.05). Conclusion Our results indicate that pp38MAPK possibly plays an important role in regulation of SGC apoptosis, following ex- posure to cisplatin.
出处 《听力学及言语疾病杂志》 CAS CSCD 北大核心 2014年第4期399-402,共4页 Journal of Audiology and Speech Pathology
基金 南京市医学科技发展课题(YKK12093)资助
关键词 螺旋神经节细胞 顺铂 凋亡 磷酸化p38MAPK蛋白 磷酸化ERK蛋白 Spiral ganglion celI(SGC) Cisplatin Apoptosis pp38MAPK pERK
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