慢性非细菌性前列腺炎(CNP)是好发于男性青壮年的常见病，该病患病率高，治愈率低，且易复发，严重危害患者身心健康，发病机制尚不明确。研究表明，T淋巴细胞亚群在CNP的发病中起关键作用，其功能与Ca2+电生理活动和mTOR通路密切相关。mTOR是机体免疫和炎症的关键调控中枢，其功能受Ca2+的信号调节，但具体机制尚不清楚。本课题组前期发现Ca2+与CNP发病机制密切相关，且mTOR通路促进CNP的发生发展，提示Ca2+通过mTOR途径调控T淋巴细胞亚群失衡是CNP的可能发病机制。本项目拟借助CNP大鼠模型，研究CNP中T淋巴细胞亚群功能及相关细胞因子变化；探讨Ca2+和mTOR通路调控T淋巴细胞亚群在CNP发病中的作用；研究Ca2+通过mTOR途径对CNP中T淋巴细胞亚群失衡调控机制；揭示CNP发病机制的调控网络和关键分子。为其发病机制提供新的理论依据，为CNP防治提供新的策略与作用靶点。

Chronic nonbacterial prostatitis(CNP) has become a common disease in young man, it has a significant morbidity, low cure rate and easy recurrence, and severely threatens male health and life quality, but the mechnaism of CNP remains unknown. Some studies indicate that T lymphocyte subsets cells are play key role in CNP, and T lymphocyte subsets cells are relate with electrophysiological activity of Ca2+ and mTOR pathway. mTOR is key role in immunity and inflammation, and regulated by Ca2+,and the mechnaism remains unknown. We previously study show that the mechanism of chronic nonbacterial prostatitis is associated with Ca2+ channel, and mTOR pathway promote the development of CNP, it suggest that Ca2+ mediate mTOR regulate the function imbalance of T lymphocyte subsets cells may be the mechnaism of CNP. So, we will intend to study the function of T lymphocyte subsets cells and relevant cytokines, applying the animal models of CNP; exploring to the T lymphocyte subsets cells in CNP with Ca2+ and mTOR; investigating the mechnaisms Ca2+ mediate mTOR regulate the function imbalance of T lymphocyte subsets cells in CNP;revaling its mechanisms of the key molecular and regulatory net, it provide the new theoretical basis of mechanisms in CNP, and provide the new strategies and targets in CNP