ERK-MAPK通路在DBP致大鼠睾丸缝隙连接损伤中作用

发布时间：2018-03-22 01:19

本文选题：邻苯二甲酸二丁酯(DBP)　切入点：支持细胞　出处：《中国公共卫生》2017年02期 　论文类型：期刊论文

【摘要】：目的探讨邻苯二甲酸二丁酯(DBP)对大鼠睾丸的损害作用及与细胞外调节蛋白激酶(ERK)信号通路激活、缝隙连接损伤关联性。方法 SD大鼠随机分为3个DBP剂量组(50、500、1 000 mg/kg)和溶剂对照组,经口灌胃染毒,每日1次,持续5周。酶联免疫吸附试验检测大鼠血清卵泡刺激素(FSH)、黄体生成素(LH)、睾酮等生殖激素水平;精子分析仪分析精子密度、活率和总畸形率;苏木素-伊红染色法观察睾丸组织结构变化;Western blot法检测ERK1/2和p-ERK蛋白表达;RT-PCR法检测缝隙连接蛋白43(Cx43)mRNA表达。结果与对照组比较,中、高剂量DBP组大鼠血清睾酮水平[(6.65±0.97)、(3.57±0.54)nmol/L]明显降低(P0.05),高剂量DBP组大鼠精子密度(64.71±11.36)10~5个/mL显著降低(P0.05),中、高剂量DBP组大鼠精子总畸形率[(13.64±1.68)%、(19.54±2.86)%]明显升高(P0.05);随DBP剂量升高大鼠睾丸组织结构损伤程度增加;与对照组比较,中、高剂量DBP组大鼠睾丸组织中p-ERK表达明显升高,各剂量DBP组大鼠睾丸组织中Cx43 mRNA表达均明显下降,差异具有统计学意义(P0.05)。结论 DBP可激活ERK通路、下调Cx43表达,引起大鼠睾丸组织结构和功能损伤。
[Abstract]:Objective to investigate the damage effect of dibutyl phthalate (DBP) on rat testis and its activation with extracellular regulated protein kinase (ERK) signaling pathway. Methods Sprague-Dawley rats were randomly divided into three DBP groups (50 500 mg / kg) and solvent control group. For 5 weeks, the levels of serum FSH, LHH, testosterone were detected by Elisa, sperm density, motility and total abnormality rate were analyzed by sperm analyzer. The changes of testicular tissue structure were observed by hematoxylin and eosin staining. The expression of ERK1/2 and p-ERK protein was detected by Western blot. The expression of gap junction protein 43(Cx43)mRNA was detected by RT-PCR. The serum testosterone level of rats in the high dose DBP group [6.65 卤0.97 + 3.57 卤0.54)nmol/L] significantly decreased P0.05A, while in the high-dose DBP group the sperm density was 64.71 卤11.36c10 ~ 5 / mL significantly lower than that in the control group. The total sperm deformity rate of rats in high dose DBP group [13.64 卤1.68 + 19.54 卤2.86%] was significantly increased, and the degree of testicular tissue structure damage increased with the increase of DBP dose. Compared with the control group, the expression of p-ERK in testis of high dose DBP group was significantly higher than that of control group. The expression of Cx43 mRNA in testis of rats with different doses of DBP decreased significantly (P 0.05). Conclusion DBP can activate the ERK pathway, down-regulate the expression of Cx43 and damage the structure and function of rat testis.
【作者单位】：北华大学公共卫生学院环境卫生学教研室;
【基金】：吉林省科技发展计划项目(201205038,20130101141JC) 吉林省教育厅计划项目(2014211)
【分类号】：R114

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