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Erectile dysfunction (ED) is a major complication of diabetes, and many diabetic men with ED are refractory to common ED therapies. Adipose tissue-derived stem cells (ADSCs) have been shown to improve erectile function in diabetic animal models. However, inadequate cell homing to damaged sites has limited their efficacy. Therefore, we explored the effect of ADSCs labeled with superparamagnetic iron oxide nanoparticles (SPIONs) on improving the erectile function of streptozotocin-induced diabetic rats with an external magnetic field. We found that SPIONs effectively incorporated into ADSCs and did not exert any negative effects on stem cell properties. Magnetic targeting of ADSCs contributed to long-term cell retention in the corpus cavernosum and improved the erectile function of diabetic rats compared with ADSC injection alone. In addition, the paracrine effect of ADSCs appeared to play the major role in functional and structural recovery. Accordingly, magnetic field-guided ADSC therapy is an effective approach for diabetes-associated ED therapy.

Erectile dysfunction is a common complication of diabetes mellitus, and the pathogenesis of diabetic erectile dysfunction is very complicated, involving neuropathy, neurotransmitters, vasculopathy, vasoactive mediators, metabolism, endocrine and so on. Diabetes mellitus can cause oxidative stress, which plays an important role in the pathogenesis of diabetic complications. This review aims at the role of oxidative stress in the pathogenesis of diabetic erectile dysfunction.

Diabetic erectile dysfunction (DED) is a multifactor syndrome, which involves vascular disease, neuropathy, metabolic control, nutrition, endocrine disorders, psychogenic factors, and anti-diabetes drugs. Among all these factors, vascular disease plays a very important role. In the development of diabetic vasculopathy, some vasomotion factors and growth factors undergo conspicuous changes, which may be significantly correlated with the development of diabetic erectile dysfunction.

Neurotrophins play significant roles in the development, differentiation and regeneration of many neurons. The abnormal changes of neurotrophins are one of the nosogenesis of diabetic peripheral neuropathy. Erectile dysfunction (ED) in diabetes is multifactorial and one of the most important causes is the injury of pelvic splanchnic nerves. Neurotrophins therapy shows exact effects on ED with pelvic splanchnic nerves injured. Recent researches indicates that the same treatment has the similar therapeutic effects on the ED animals with diabetes. Neurotrophins therapy develops a new way for us to cure the ED with diabetes.

Objective: To investigate the changes of angiotensin II (Ang II) and its receptors in male rats with diabetic erectile dysfunction (DED) so as to study its effects., Methods: Out of 40 male SD rats, 30 were taken at random for diabetic models. After 8 weeks, the rats with erectile dysfunction were selected from these models. All the rats were divided into 3 groups: control ( n = 10), diabetes mellitus( DM, n = 9) and DED (n = 8). For each rat, the Ang II levels in the blood and homogenate prepared from part of the isolated penile tissues were determined respectively, and the Ang II receptors of the rest of the penile tissues were analyzed through immunohistochemical (IHC) assay., Results: Compared with the control group, Ang II levels in the blood and penile tissues in the DM group, and that in the blood of the DED group were very high and the differences were statistically significant (P < 0.05). Ang II in the penile tissues of the DED increased sharply (P < 0.01). The receptors of Ang II changed contrariwise to the level of Ang ll., Conclusion: Ang II may play an important role in the pathogenesis of DED, and the Ang II antagonist or inhibitor of the angiotensin-converting enzyme (ACEI) may become a therapeutic method for DED in the future.