Abstract
Osteoporosis is a common disease caused by an imbalance of processes between bone resorption by osteoclasts and bone formation by osteoblasts in postmenopausal women. The roots of Gentiana lutea L. (GL) are reported to have beneficial effects on various human diseases related to liver functions and gastrointestinal motility, as well as on arthritis. Here, we fractionated and isolated bioactive constituent(s) responsible for anti-osteoporotic effects of GL root extract. A single phytochemical compound, loganic acid, was identified as a candidate osteoprotective agent. Its anti-osteoporotic effects were examined in vitro and in vivo. Treatment with loganic acid significantly increased osteoblastic differentiation in preosteoblast MC3T3-E1 cells by promoting alkaline phosphatase activity and increasing mRNA expression levels of bone metabolic markers such as Alpl, Bglap, and Sp7. However, loganic acid inhibited osteoclast differentiation of primary-cultured monocytes derived from mouse bone marrow. For in vivo experiments, the effect of loganic acid on ovariectomized (OVX) mice was examined for 12 weeks. Loganic acid prevented OVX-induced bone mineral density loss and improved bone structural properties in osteoporotic model mice. These results suggest that loganic acid may be a potential therapeutic candidate for treatment of osteoporosis.
Highlights
Introduction in published maps and institutionalOsteoporosis is a progressive skeletal disorder characterized by dysregulation of bone remodeling, resulting in systemic reduction of bone mass and a high risk of bone fracture [1].In elderly or postmenopausal women, osteoporosis occurs frequently because of estrogen deficiency, which plays a critical role in bone homeostasis [2,3]
To examine osteoprotective effects of Gentiana lutea L. (GL) root extract, we investigated alkaline phosphatase (ALP) activity in osteoblast cells and tartrate-resistant acid phosphatase (TRAP) activity in osteoclast cells
The results indicated that a 30% ethanol extract of GL root promoted ALP activity in MC3T3-E1 preosteoblast cells, whereas it inhibited TRAP activity in primary-cultured osteoclast cells (Supplementary Figure S1)
Summary
Osteoporosis is a progressive skeletal disorder characterized by dysregulation of bone remodeling, resulting in systemic reduction of bone mass and a high risk of bone fracture [1]. In elderly or postmenopausal women, osteoporosis occurs frequently because of estrogen deficiency, which plays a critical role in bone homeostasis [2,3]. Deficiency of female hormones trigger an abnormal bone remodeling process between bone formation (osteoblasts) and resorption (osteoclasts) [4]. Osteoblasts are derived from mesenchymal stem cells and play a central role in the regulation of bone mineralization and formation [5,6]. Impaired regulation between bone formation and resorption leads to inappropriate bone remodeling processes with serious bone loss, resulting in osteopenia and osteoporosis [8,9].
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