Research on Protective Mechanism of Antioxidant Sodium TanshinoneⅡA Sulfonate on Erectile Function in Hyperlipidemia Rats

Abstract

Objective: Sodium tanshinone ⅡA sulfonate (STS) is recognized to be beneficial to oxidative stress (OS). However, it is unclear whether it protects erectile function by antioxidative stress and maintains the contractile phenotype of cavernosal smooth muscle cells (CCSMCs) in hyperlipidemia-induced erectile dysfunction (ED) rats. Therefore, this research aimed to assess the protective effect and the mechanism of STS on cavernous smooth muscle cells in hyperlipidemia-related ED. Methods: This study assessed erectile function using the intracavernous pressure (ICP)/mean arterial pressure (MAP) ratio. The phenotypic and oxidative-related markers were determined using western blot and immunohistochemistry assays. Sprague-Dawley rats were grouped as a normal control (NC) and four hyperlipidemia groups, including hyperlipidemia rats (HR), hyperlipidemia with saline (HR+NS), hyperlipidemia with 300 mg/kg N-acetylcysteine (HR+NAC), and hyperlipidemia rats with 10 mg/kg sodium tanshinone ⅡA sulfonate (HR+STS). After 4 months, all rats were sacrificed for serum biochemistry, OS markers, and penile histologic examinations after ICP and MAP tests. Results: The ICP/MAP ratio was significantly higher in HR+STS and HR+NAC groups than in HR and HR+NS groups (p < 0.05). Compared to the other hyperlipidemia rats, STS treatment markedly increased the expression of phenotypic proteins alpha-smooth muscle actin (α-SMA), smooth muscle myosin heavy chain (SMMHC), calponin, and Myocardin and decreased the osteopontin (OPN) expression in the penis (p < 0.05). Furthermore, we demonstrated that STS increased SOD and GSH expression while reducing MDA expression in serum and corpus cavernosum tissues compared with the HR group. Conclusions: STS treatment protected the erectile function by reducing the OS and maintaining the contractile phenotype in the CCSMCs of the hyperlipidemia-induced ED rats.