Therapeutic Potential of Salidroside in Diabetic Erectile Dysfunction: Attenuation of Oxidative Stress and Apoptosis via Upregulation of the Nrf2/HO-1 Pathway

Abstract

Abstract The primary objective of this research was to delve into the potential therapeutic advantages and intricate molecular mechanisms of salidroside in enhancing erectile function in rats afflicted with DMED, addressing both the animal and cellular dimensions. We utilized Sprague-Dawley (SD) rats to establish DMED models and conduct an in vivo investigation. The DMED rats were treated with varying doses of salidroside and the effects of different doses of Salidroside on DMED were compared. The evaluation of erectile function involved the application of electrical stimulation to the cavernous nerves and the measurement of intracavernous pressure in real time. The penile tissue underwent histological examination and was subsequently analyzed through Western blotting. Hydrogen peroxide (H2O2) was employed in the in vitro trial to induce an oxidative stress condition for the purpose of identifying alterations in cell viability. The CCK8 assay was used to measure the viability of CCSMCs treated with or without salidroside. Flow cytometry was utilized to detect alterations in intracellular reactive oxygen species (ROS). Apoptosis was assessed through Western blotting and TdT-mediated dUTP Nick-End Labeling (Tunel) staining. Ultimately, we found that the Nrf2/HO-1 signaling pathway may be upregulated by Salidroside, leading to the improvement of erectile function in diabetic male rats by alleviating oxidative stress,and reducing apoptosis in the corpus cavernosum tissue.