p38MAPK→COX2 和 NF-κB→COX2 信号通路在与年龄相关的睾酮减少中的作用。
The roles of p38 MAPK → COX2 and NF-κB → COX2 signal pathways in age-related testosterone reduction.
机构信息
Department of Histology and Embryology, Hebei Medical University, Shijiazhuang, 050017, China.
Department of Occupational and Environmental Health, Hebei Province Key Laboratory of Environment and Human Health, Hebei Medical University, Shijiazhuang, 050017, China.
出版信息
Sci Rep. 2019 Jul 22;9(1):10556. doi: 10.1038/s41598-019-46794-5.
In our study, we explored changes in the redox status and inflammatory response in the testes of the SAMP8 model of varying ages (2, 4, 8, 10 months old) compared with control mice SAMR1 by the methods of immunohistochemical staining, Western blotting, RT-PCR and Luminex multi-analyte cytokine profiling. We found that as ROS and inflammation levels increased during aging, steroidogenic enzymes (StAR and P450scc) reduced and led to the decline of testosterone production eventually. The pathways of P38 MAPK → COX2 and NF-κB → COX2 were detected by using specific inhibitors of SB203580 and Bay 11-7082 in isolated Leydig cells. These results indicated that activation of both p38 MAPK → COX2 and NF-κB → COX2 signaling pathways are functionally linked to the oxidative stress response and chronic inflammation during aging, and mediate their inhibitory effects on testosterone production.
在我们的研究中，我们通过免疫组织化学染色、Western blot、RT-PCR 和 Luminex 多因子细胞因子分析等方法，研究了不同年龄（2、4、8、10 个月）的 SAMP8 模型与对照 SAMR1 小鼠睾丸中氧化还原状态和炎症反应的变化。我们发现，随着衰老过程中 ROS 和炎症水平的升高，类固醇生成酶（StAR 和 P450scc）减少，最终导致睾酮产生下降。在分离的 Leydig 细胞中，使用特异性抑制剂 SB203580 和 Bay 11-7082 检测到 P38 MAPK→COX2 和 NF-κB→COX2 通路。这些结果表明，p38 MAPK→COX2 和 NF-κB→COX2 信号通路的激活与衰老过程中的氧化应激反应和慢性炎症有关，并介导它们对睾酮产生的抑制作用。
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