Abstract
Puerariae radix (PR) is one of the earliest and most important crude herbs used in Chinese medicine
for various medicinal purposes. PR contains a high amount of isoflavonoids, such as
daidzein and genistein, which are known to prevent bone loss induced by estrogen deficiency.
We have demonstrated that PR not only completely prevents bone loss but also significantly
increases the bone mass at high doses in ovariectomized mice without exhibiting estrogenic
action in the uterus. In this study, we examined whether PR exhibits effects on bone
loss in androgen-deficient male mice similar to estrogen-deficient female mice. Male
mice were orchidectomized (ORX) and fed a diet containing low, middle, and high doses
(5%, 10%, and 20% of diet, respectively) of PR or normal diet with subcutaneous administration
of 17β-estradiol (E2, 0.03 μg/d; Sigma, St Louis, Mo), for 4 weeks. In ORX mice, the seminal vesicle weight decreased
markedly, and it was not affected by the administration of any doses of PR and E2. The bone mineral density (BMD) of the whole femur was significantly decreased by
ORX, and the decrease in BMD was completely prevented by intake of the diet with the
low dose of PR. Intake of the diet with the middle dose of PR further normalized BMD
in ORX mice. Furthermore, the high dose of PR administration (PR20) significantly
increased BMD in ORX mice, and the potency was similar to that of E2. Morphometric analysis of the femoral metaphysis showed that intake of the diet with
the low dose of PR completely prevented the decrease in bone volume/tissue volume
and trabecular number and restored the increase in trabecular separation in ORX mice.
In addition, intake of the diet with the high dose of PR further increased bone volume/tissue
volume and trabecular number and decreased trabecular separation in ORX mice. These
results propose the possibility that estrogenic Chinese herbs such as PR can be one
of the candidates for the treatment or prevention of osteoporosis in elderly men with
hypogonadism.
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Article info
Publication history
Accepted:
May 15,
2005
Received:
March 1,
2005
Identification
Copyright
© 2005 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
