Yang Peng, Zhu Tianle, Ma Yukuai, Cao Zhi, Gao Pan, Jiang Hui, Zhang Xiansheng
The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Peking University Andrology Center, Peking University First Hospital, Beijing, China.
Andrology. 2024 Dec 20. doi: 10.1111/andr.13826.
Although some studies suggest that sleep deprivation may affect ejaculation regulation, related research is limited, and the mechanisms remain unclear.
This study aimed to explore whether sleep deprivation influences ejaculation regulation through amyloid-beta and to investigate its potential mechanisms.
Normal ejaculating rats were randomly distributed into three separate groups for the study, and treated with sleep deprivation combined with saline gavage, sleep deprivation combined with sodium butyrate gavage, and control with saline gavage. The levels of amyloid-beta and 5-HT receptors were assessed through Western blotting, PCR, and immunohistochemical techniques. The levels of interleukin-4 and serotonin (5-hydroxytryptamine) in the brain were determined by enzyme-linked immunosorbent assay.
The experiment showed that the rats in the sleep deprivation combined with saline gavage group rats had a significantly faster ejaculation compared to the control combined with saline gavage group rats. Meanwhile, sleep deprivation combined with saline gavage group had the highest levels of amyloid-beta oligomers in the brain tissue. Correlation results revealed that the levels of amyloid-beta oligomers in brain tissue were inversely related to ejaculation latency and positively associated with ejaculation frequency. Furthermore, we found that elevated levels of amyloid-beta oligomers in brain tissue led to upregulation of 5-HT receptor expression. Additionally, elevated levels of amyloid-beta oligomers in brain tissue were found to increase interleukin-4 levels, thereby reducing 5-hydroxytryptamine levels.
Sleep deprivation indeed accelerates ejaculation, and this acceleration is closely related to amyloid-beta. Sleep deprivation can increase amyloid-beta levels in brain tissue, mediating a decrease in 5-hydroxytryptamine levels and overexpression of 5-HT receptors, thereby accelerating ejaculation.
There is a significant correlation between elevated amyloid-beta levels in brain tissue because of sleep deprivation and accelerated ejaculation. This study's main findings offer insights into the development of acquired premature ejaculation linked to poor sleep and establish a theoretical framework for investigating potential treatments for this condition.
尽管一些研究表明睡眠剥夺可能会影响射精调节，但相关研究有限，其机制仍不清楚。
本研究旨在探讨睡眠剥夺是否通过β-淀粉样蛋白影响射精调节，并研究其潜在机制。
将正常射精的大鼠随机分为三组进行研究，分别给予睡眠剥夺联合生理盐水灌胃、睡眠剥夺联合丁酸钠灌胃以及生理盐水灌胃作为对照。通过蛋白质免疫印迹法、聚合酶链反应和免疫组织化学技术评估β-淀粉样蛋白和5-羟色胺受体水平。采用酶联免疫吸附测定法测定大脑中白细胞介素-4和血清素（5-羟色胺）水平。
实验表明，睡眠剥夺联合生理盐水灌胃组大鼠的射精速度明显快于生理盐水灌胃对照组大鼠。同时，睡眠剥夺联合生理盐水灌胃组大鼠脑组织中β-淀粉样蛋白寡聚体水平最高。相关性结果显示，脑组织中β-淀粉样蛋白寡聚体水平与射精潜伏期呈负相关，与射精频率呈正相关。此外，我们发现脑组织中β-淀粉样蛋白寡聚体水平升高导致5-羟色胺受体表达上调。另外，还发现脑组织中β-淀粉样蛋白寡聚体水平升高会增加白细胞介素-4水平，从而降低5-羟色胺水平。
睡眠剥夺确实会加速射精，且这种加速与β-淀粉样蛋白密切相关。睡眠剥夺可增加脑组织中β-淀粉样蛋白水平，介导5-羟色胺水平降低和5-羟色胺受体过表达，从而加速射精。
因睡眠剥夺导致的脑组织中β-淀粉样蛋白水平升高与射精加速之间存在显著相关性。本研究的主要发现为与睡眠不佳相关的后天性早泄的发展提供了见解，并为研究该病症的潜在治疗方法建立了理论框架。
