N-acetylcysteine Ameliorates the Erectile Dysfunction Caused by Chronic Intermittent Hypoxia in Rats: Partly Involvement of Endoplasmic Reticulum Stress - 01/10/15
Abstract |
Objective |
To conduct a study using a rodent model of chronic intermittent hypoxia (CIH) to define whether endoplasmic reticulum stress (ERS) is involved in the CIH-induced apoptosis of penile tissue and erectile dysfunction (ED), and whether treatment with N-acetylcysteine (NAC) alleviates pathological variations in corpus cavernosa. Previous work has prompted that CIH acted as the major trigger linking obstructive sleep apnea syndrome and ED.
Materials and Methods |
Five-month-old Sprague-Dawley male rats were subjected to 8 hours of intermittent hypoxia per day, with or without NAC for 5 weeks. Erectile function, apoptosis of penile tissue, levels of ERS-associated proapoptotic effectors, and nitric oxide (NO) and nitric oxide synthase (NOS) activity were determined.
Results |
Treatment with NAC inhibited apoptosis of penile tissue, the expressions of ERS-related products: BIP, CHOP, caspase12, and Bax, NO, and endothelial NOS. Administration of NAC before CIH significantly improved the CIH-induced impaired erectile function.
Conclusion |
Our results show that pre-CIH NAC administration ameliorates the ED following CIH partly by alleviating CIH-induced ERS and cell apoptosis via regulating the expressions of BIP, CHOP, caspase12, and Bax.
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| Financial Disclosure: The authors declare that they have no relevant financial interests. |
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| Funding Support: This study was funded by the National Natural Science Foundation of PR China (grants 81370185). |
Vol 86 - N° 4
P. 844.e7-844.e14 - octobre 2015 Retour au numéro
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