JOURNAL ARTICLE

[Sodium ferulate treatment and interventional mechanism reverse erectile dysfunction in streptozotocin-induced diabetic rats]

Xiao-Hong Xu, Fu-Qing Tan, Tong-Feng Zhao, Hua Hu, Kun Xiao, Wei Gu
Zhonghua Yi Xue za Zhi [Chinese medical journal] 2009 June 23, 89 (24): 1711-3
19957533

OBJECTIVE: To investigate the effect and mechanism of sodium ferulate (SF) on reversing erectile dysfunction in diabetes mellitus (DM) rats.

METHODS: Forty-four male adult Sprague-Dawley rats were induced for diabetes by an intraperitoneal injection of streptozotocin. Then the successful models were randomly divided into DM + SF group and DM group (22 rats each respectively). The rats in DM +SF group were treated with sodium ferulate (100 mg x kg(-1) x d(-1)) through a daily gastric lavage. At Week 12, the erectile function of all rats was evaluated and serum samples were harvested. The SOD, CAT, NOS, MDA and NO levels in corpus cavernosum and serum were all measured. The pathologic change in penile cavernous body was observed microscopically.

RESULTS: The diabetic rat models were successfully established. The erectile function was much better in normal control group and DM + SF group than that in DM group. And the penile erection rates in three groups were 100%, 66% and 22% respectively. The activity levels of SOD, CAT and NOS were markedly decreased in DM group as compared to those in normal control group and DM + SF group (P < 0.01). The NO content was approximately equal in normal control group and DM + SF group (112 +/- 28) nmol/ml vs (137 +/- 25) nmol/ml. But both were much higher than that in DM group (56 +/- 10) nmol/ml, both P < 0.01. The MDA content was markedly increased in DM group as compared to those in normal control group and DM + SF group (both P < 0.01). Microscopically, muscle fibers in penile cavernous body arranged disorderly, muscular mantle damaged and desmoplasia scattered among muscle fibers in DM group.

CONCLUSION: Sodium ferulate may play interventional roles in reversing diabetic erectile dysfunction through metabolic regulation of free radicals, antagonism of oxidative insults and enhancement of NO production.

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