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Is Nitric Oxide a Mediator of the Effects of Low-Intensity Electrical Stimulation on Bone in Ovariectomized Rats?

Low-intensity electrical stimulation (LIES) may counteract the effects of ovariectomy (OVX) on nitric oxide synthase (NOS) expression, osteocyte viability, bone structure, and microarchitecture in rats (Lirani-Galvão et al., Calcif Tissue Int 84:502–509, 2009). The aim of the present study was to in...

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Published in:Calcified tissue international 2010-07, Vol.87 (1), p.52-59
Main Authors: Lirani-Galvão, A. P. R., Lazaretti-Castro, M., Portero-Muzy, N., Bergamaschi, C. T., Silva, O. L., Carvalho, A. B., Delmas, P. D., Chavassieux, P.
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Language:English
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Summary:Low-intensity electrical stimulation (LIES) may counteract the effects of ovariectomy (OVX) on nitric oxide synthase (NOS) expression, osteocyte viability, bone structure, and microarchitecture in rats (Lirani-Galvão et al., Calcif Tissue Int 84:502–509, 2009). The aim of the present study was to investigate if these effects of LIES could be mediated by NO. We analyzed the effects of NO blockage (by l -NAME) in the response to LIES on osteocyte viability, bone structure, and microarchitecture in OVX rats. Sixty rats (200–220 g) were divided into six groups: sham, sham- l -NAME (6 mg/kg/day), OVX, OVX- l -NAME, OVX-LIES, and OVX-LIES- l -NAME. After 12 weeks, rats were killed and tibiae collected for histomorphometric analysis and immunohistochemical detection of endothelial NOS (eNOS), inducible NOS (iNOS), and osteocyte apoptosis (caspase-3 and TUNEL). In the presence of l -NAME, LIES did not counteract the OVX-induced effects on bone volume and trabecular number (as on OVX-LIES). l -NAME blocked the stimulatory effects of LIES on iNOS and eNOS expression of OVX rats. Both l -NAME and LIES decreased osteocyte apoptosis. Our results showed that in OVX rats l -NAME partially blocks the effects of LIES on bone structure, turnover, and expression of iNOS and eNOS, suggesting that NO may be a mediator of some positive effects of LIES on bone.
ISSN:0171-967X
1432-0827
DOI:10.1007/s00223-010-9357-0