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

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.

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.

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.

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.