Here’s another line of research for treating ED – hydrogen-rich saline (HRS). This study from China found that HRS helps fight ED in the diabetic rat model.
J Urol. 2012 Dec 4. pii: S0022-5347(12)05812-0. doi: 10.1016/j.juro.2012.12.001. [Epub ahead of print] Protective Effects of Hydrogen-rich Saline against Erectile Dysfunction in a Streptozotocin-Induced Diabetic Rat Model.
Source: Department of Urology, the Third Affiliated Hospital of Soochow University, Changzhou 213000, Jiangsu Province, China.
Hydrogen has anti-oxidative-stress and anti-inflammatory effects. In the present study, we investigated the effect of hydrogen on erectile dysfunction (ED) in streptozotocin (STZ)-induced diabetic rats. Rats with diabetes mellitus (DM) in the hydrogen-rich saline (HRS) group were fed saturated hydrogen saline by intragastric administration (5 ml/kg/d) for 8 weeks (n = 8).
MATERIALS AND METHODS:
Diabetes was induced in SpragueDawley rats by a single intravenous injection of STZ. The diabetic rats were then randomized into a DM group and a DM hydrogen saline group; the latter were fed saturated hydrogen saline by intragastric administration (5 ml/kg/d) for 8 weeks (n = 8). At the end of week 8, erectile function was assessed by measuring the rise in intracavernous pressure (ICP) following cavernous nerve electrostimulation. Nitric oxide synthase (NOS) activity, malondialdehyde (MDA) content, 8-hydroxydeoxyguanosine (8-OhdG), and nitrite and nitrate (NOx) levels were measured in corpus cavernosum tissues. Immunolocalization of the endothelial NO synthase (eNOS) protein in corpus cavernosum tissues was detected using immunohistochemistry. Protein expression of eNOS, Bcl-2, and Bax was determined by Western blotting. eNOS, Bcl-2, and Bax mRNA levels were determined using real-time reverse transcription polymerase chain reaction methods.
Oxidative stress is involved in the pathophysiological mechanism of ED. Maximum ICP in diabetic rats decreased significantly compared to that in controls. Maximum ICP increased significantly compared to that in untreated diabetic rats after treatment with HRS. Decreased levels of NOS activity, NOx and eNOS expression, as well as elevated levels of 8-OhdG and MDA were found in the DM group compared with those in the control group. HRS treatment improved NOS activity and MDA, NOx, and 8-OHdG levels in the corpus cavernosum of diabetic rats. Decreased eNOS expression in diabetic rats was ameliorated by HRS treatment. In addition, apoptosis in the diabetic rat corpus cavernosum was enhanced significantly compared with that in the control group. HRS therapy may reduce apoptosis in corpus cavernosum tissues. Furthermore, HRS ameliorated ED in diabetic rats by inhibiting oxidative stress and apoptosis.
HRS treatment effectively improved erectile function in a STZ-induced diabetic rat ED model.