Abstract
Oleanolic acid (OA) is a triterpenoid with reported bone anti-resorption activities. The present study aimed to characterize its bone protective effects in vivo and to study its effects on vitamin D metabolism, both in vivo and in vitro. OA significantly increased bone mineral density, improved micro-architectural properties, reduced urinary Ca excretion, increased 1,25(OH)2D3 and renal CYP27B1 mRNA expression in mature C57BL/6 ovariectomised (OVX) mice. OA also improved bone properties, Ca balance, and exerted modulatory effects on renal CYP27B1 and CYP24A1 expressions in aged normal female Sprague–Dawley rats. In addition, OA significantly increased renal CYP27B1 mRNA and promoter activity, and suppressed CYP24A1 mRNA and protein expressions in human proximal tubule HKC-8 cells. OA exerted bone protective effects in mature OVX mice and aged female rats. This action on bone might be, at least in part, associated with its effects on Ca and vitamin D metabolism. The present findings suggest that OA is a potential drug candidate for the management of postmenopausal osteoporosis.
Highlights
Osteoporosis is a metabolic bone disease that increases fracture risk in the elderly and poses significant social and economic burden to the world’s population
Serum and urinary phosphorus levels were not altered by OVX or any intervention, while urinary calcium loss induced by OVX was suppressed in mice treated with E2 (p < 0.05 vs. OVX) and with Oleanolic acid (OA)
Serum 1,25(OH)2 D3 levels were significantly increased in OVX mice treated with OA at a high dose (p < 0.05 vs. OVX, Table 2), but were not altered in other treatment groups
Summary
Osteoporosis is a metabolic bone disease that increases fracture risk in the elderly and poses significant social and economic burden to the world’s population. The worldwide estimated osteoporosis-related fracture rate is around 40% in aged women and about 13% in men [1]. Estrogen deficiency [3] are the two major leading causes of osteoporosis. The age-related changes in calcium homeostasis may contribute to the chronic depletion of calcium from bone [4]. The impaired intestinal calcium absorption during aging is believed to be the consequence of the age-related decline in renal 1,25(OH) D3 production and intestinal vitamin D receptor (VDR). The reduction of estrogen level during menopausal transition contributes to rapid bone loss in women, with an average decline of 10% bone mineral density (BMD) in the five years around menopause [3]. The estrogen deficiency-induced bone loss in postmenopausal women is complicated by the age-induced abnormalities in the vitamin
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