Salidroside inhibits hypoxia-induced phenotypic modulation of corpus cavernosum smooth muscle cells in vitro / 中华男科学杂志
National Journal of Andrology
;
(12): 727-731, 2013.
Article
in Chinese
| WPRIM
| ID: wpr-350828
ABSTRACT
<p><b>OBJECTIVE</b>To explore the effects of salidroside on the phenotypic modulation of corpus cavernosum smooth muscle cells (CCSMC) in hypoxic SD rats.</p><p><b>METHODS</b>CCSMCs were cultured in vitro and identified by immunohistochemistry. The cells were divided into six groups normal control (21% O2), hypoxia (1% O2), hypoxia + salidroside 1 mg/L, hypoxia + salidroside 3 mg/L, hypoxia + salidroside 5 mg/L and hypoxia + PGE1 0.4 microg/L, and then cultured for 48 hours. The relative expressions of alpha-actin and osteopontin (OPN) in each group were determined by RT-PCR.</p><p><b>RESULTS</b>The in vitro cultured CCSMCs grew well, with anti-alpha-smooth muscle actin monoclonal antibodies immunohistochemically positive. The relative expression of alpha-actin was markedly decreased while that of OPN remarkably increased in the hypoxia group as compared with the normal control group (P < 0.01). The hypoxia + salidroside 5 mg/L group showed a significantly higher expression of alpha-actin and lower expression of OPN than the hypoxia group (P < 0.01), but exhibited no significant differences from the hypoxia + PGE group (P > 0.05).</p><p><b>CONCLUSION</b>Hypoxia can reduce the relative expression level of alpha-actin and increase that of OPN in the CCSMCs of SD rats, namely, induce their phenotypic modulation from the contraction to the non-contraction type. Salidroside can restrain hypoxia-induced phenotypic modulation of CCSMCs, and its inhibitory effect at 5 mg/L is similar to that of PGE1.</p>
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Penis
/
Pharmacology
/
Phenols
/
Cell Hypoxia
/
Cells, Cultured
/
Actins
/
Rats, Sprague-Dawley
/
Cell Biology
/
Myocytes, Smooth Muscle
/
Osteopontin
Limits:
Animals
Language:
Chinese
Journal:
National Journal of Andrology
Year:
2013
Type:
Article
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