Study on the mechanism of erectile dysfunction in D-galactose induced aging rats: the construction of aging model.

Abstract

Background: The incidence of erectile dysfunction (ED) rises sharply with age, which has brought a huge social burden. The exploration of aging-related ED is hindered due to the limitations of natural aging models. As an ideal inducer of accelerated aging models, the mechanism of D-galactose (D-gal) in ED has not been fully elucidated. Therefore, this study aimed to verify the feasibility of aging-related ED induced by D-gal and explore its potential mechanism.

Methods: Primary corpus cavernosum smooth muscle cells (CCSMCs) and human umbilical vein endothelial cells (HUVECs) were incubated with concentration gradients of D-gal. Meanwhile, aging rat models were established via intraperitoneal and subcutaneous injection of D-gal, and the erectile function of all subjects was measured by electrical stimulation. Samples from both cells and animals were then collected for subsequent detection.

Results: Cellular senescence was confirmed in both cells and was accompanied by oxidative stress, mitochondrial dysfunction, and cell cycle arrest in vitro. The erectile function of rats treated with D-gal was affirmed to be impaired compared with normal rats. In addition to the above-mentioned pathological alterations, tissue fibrosis was also associated with D-gal administration in vivo. Moreover, no significant difference was found between the two administration methods in inducing senescence of rats.

Conclusions: D-gal could promote the progression of aging-related ED, accompanied by the exacerbation of oxidative stress, mitochondrial dysfunction, cell cycle arrest, and fibrosis. Our data suggested that D-gal may be an ideal mediator for the induced model of aging-related ED, which could facilitate preclinical exploration of this disease.