基于H2S/NRF2/HO-1/Myocardin通路探讨丹参酮IIA磺酸钠对高脂血症ED大鼠勃起过程中的作用及机制研究

丹参酮IIA磺酸钠（STS）具有抑制血管平滑肌细胞增殖，清除自由基等作用，在心血管系统疾病广泛应用。阴茎海绵体平滑肌细胞（CCSMCs）表型转化是导致高脂血症大鼠勃起功能障碍（ED）的重要病理基础，我们前期研究证实STS能改善高脂血症ED大鼠勃起功能，提高H2S的表达并上调myocardin的活性而抑制CCSMCs发生表型转化，但它是否通过H2S信号通路启动了抗氧化应激并影响Myocardin调控CCSMCs表型，进而影响其勃起功能，以及它们之间的信号通路网络关系不清楚。故我们推测STS可能通过H2S信号通路介导的抗氧化应激影响myocardin的功能而抑制高脂血症ED大鼠CCSMCs发生表型转化，进而改善其勃起功能。研究结果有助于完善阴茎勃起调控过程中的信号通路理论，最终为明确中医药改善高脂血症ED的分子机制提供实验依据。

Sodium tanshinone IIA sulfonate (STS) can inhibit the proliferation of vascular smooth muscle cells and scavenge free radicals, which is widely used in cardiovascular diseases. Phenotypic modulation of corpus cavernosum smooth muscle cells (CCSMCs) plays a key role in the pathogenesis of hyperlipidemia rats with erectile dysfunction (ED). Our previous studies have confirmed that STS can improve the erectile function of ED rats with hyperlipidemia, increase the expression of H2S and up-regulate the activity of myocardin, thus inhibiting the phenotypic modulation of CCSMCs. However, it is unclear whether it activates anti-oxidative stress through H2S signaling pathway and influences Myocardin to regulate the phenotype of CCSMCs, thereby affecting its erectile function and the relationship between them in the signaling pathway network. Therefore, we speculated that STS might affect the function of myocardin through the anti-oxidative stress mediated by H2S signaling pathway and inhibit phenotypic modulation of CCSMCs in ED rats with hyperlipidemia, thereby improving their erectile function. Our experimental results will further perfect the theory of signaling pathway in the process of regulating penis erectile and provide experimental date for clarifying the molecular mechanism of Chinese medicine to improve ED in hyperlipidemia.