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Enhanced effects of salidroside on erectile function and corpora cavernosa autophagy in a cavernous nerve injury rat model.

Miaoyong YeFan ZhaoKe MaKang ZhouJianxiong MaHuiying FuZengbao XuWenjie HuangWenzhi WangJianfeng ZhaoBo-Dong Lv
Published in: Andrologia (2021)
We explored the efficacy and mechanisms of salidroside treatment for erectile dysfunction induced by bilateral cavernous nerve injury (BCNI). Forty male rats were divided into four groups as follows: sham (cavernous nerves exposed only) (S); BCNI (M); BCNI + rapamycin (M + rapamycin); and BCNI + salidroside (M + salidroside). Erectile function in the rats was measured by intracavernosal pressure. Penile tissue was harvested for transmission electron microscopy, immunohistochemistry, immunofluorescence, Masson's trichrome staining, haematoxylin-eosin staining, TdT-mediated dUTP Nick End Labeling and western blotting. The M group exhibited a decrease in erectile responses and increased apoptosis and fibrosis compared to these in the S group. Meanwhile, nerve content and the penile atrophy index were also decreased in the M group. Treatment with salidroside and rapamycin for 3 weeks partially restored erectile function and significantly attenuated corporal apoptosis, fibrosis, nerve content and penile atrophy in the M group. Moreover, the autophagy level was further enhanced in the M + salidroside group, which was the same as that in the positive observation group (M + rapamycin). Salidroside treatment not only improved erectile function in rats with BCNI, but also inhibited apoptosis and fibrosis and ameliorated the loss of nerve content and endothelial and corpus cavernosum smooth muscle cells by promoting protective autophagy.
Keyphrases
  • endoplasmic reticulum stress
  • oxidative stress
  • cell death
  • peripheral nerve
  • signaling pathway
  • cell cycle arrest
  • prostate cancer
  • replacement therapy
  • electron microscopy
  • cell proliferation
  • flow cytometry