早产是导致婴儿发病率及死亡率的首要原因，但目前尚无防治早产的有效手段，其原因在于早产的发生机制未明确。现已知感染是早产发生的主要原因。在我们前期工作中，向孕鼠腹腔注射脂多糖（LPS）成功建立了小鼠感染性早产模型，并发现LPS通过激活NF-κB信号通路上调T型钙通道的表达，同时LPS能够激活T型钙通道使细胞内钙浓度增加。由此我们推测T型钙通道可能参与了LPS诱导的感染性早产的发生。本研究拟收集人的早产子宫平滑肌组织，通过细胞培养、PCR、western-blot、免疫组化等分子生物学方法及膜片钳等电生理技术，进一步证实T-型钙通道在早产中的作用，并明确T型钙通道在早产发生中的具体机制。早产的治疗是多年来困扰产科的棘手问题。钙离子通道是子宫收缩的钙信号传导的的必经之路，从T-型钙离子通道入手，研究早产的发生机制，将为发现新的治疗早产的有效药物及靶点提供理论依据。

Preterm birth is the leading cause of infant morbidity and mortality, but at present there is no effective method to prevent preterm birth, the reason is that the mechanism of preterm delivery is not clear. Infection is the main cause of premature delivery. In our previous work, we injected lipopolysaccharide (LPS) into pregnant rats' abdominal cavity and successfully established infected preterm model. We found that LPS can upregulate the expression of T type calcium channel through NF- kappa B signaling pathway, LPS can also activate T type calcium channel to increase intracellular calcium concentration. Thus we speculate that T type calcium channel may be involved in the occurrence of preterm birth induced by LPS. This study intends to collect people's uterine smooth muscle tissue of preterm birth, through molecular biology methods and electrophysiological technique, such as cell culture, PCR, Western-blot, immunohistochemistry and patch clamp, will further prove the role of T- type calcium channel in preterm labor and clear the specific mechanism of T type calcium channel in preterm labor. Preventing and curing preterm labor is always a thorny problem in obstetrics. Calcium ion channel is the only and final way of calcium signal transduction of uterine contraction, starting from T- type calcium channel to study the mechanism of premature delivery, will provide a theoretical basis and a new target for finding effective drug to treat preterm birth.