Abstract
In Asia, extracts of Lysimachia christinae have been used for liver or urinogenital system-related diseases in traditional medicine. In this study, we investigated the effects of the water extract of L. christinae (WELC) on receptor activator of nuclear factor-kappa Β ligand (RANKL)-induced osteoclastic differentiation of bone marrow macrophages, and on osteoporosis and obesity in ovariectomy mice. RANK signaling pathways related to osteoclast differentiation were examined by real-time polymerase chain reaction (PCR) and western blot analysis. Additionally, we performed micro-computed tomography to assess trabecular bone loss, histological analysis for fat accumulation in adipose, liver, and bone tissues, and phytochemical profiling for WELC characterization. WELC significantly inhibited osteoclast differentiation by downregulating RANKL-induced mitogen-activated protein kinase (MAPK)/c-Fos/nuclear factor of activated T-cells (NFAT) signaling in osteoclast precursors and ovariectomy-induced trabecular loss by suppressing osteolcastic bone resorption. WELC markedly decreased ovariectomy-induced body weight gain and fat accumulation in adipose, liver, and bone tissues. Furthermore, ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC–MS/MS) identified 16 phytochemicals in WELC when compared with the mass fragmentation of standard chemicals. Collectively, these results suggest that WELC might possess beneficial effects on postmenopausal osteoporosis by inhibiting osteoclast differentiation and obesity by suppressing fat accumulation.
Highlights
Menopause and estrogen decline induce significant physiological alterations in women’s health, including the development of osteoporosis and obesity
water extract of L. christinae (WELC) Inhibits RANK Signaling during Osteoclast Differentiation
bone marrow-derived macrophage cells (BMMs) are precursor cells possessing the potential to differentiate into osteoclasts in the presence of receptor activator of nuclear factor-kappa B ligand (RANKL)
Summary
Menopause and estrogen decline induce significant physiological alterations in women’s health, including the development of osteoporosis and obesity. In the bone remodeling unit, estrogen participates in the regulation of bone resorption by osteoclasts and bone formation by osteoblasts [1,2]. Estrogen loss increases the bone resorption rate rather than the bone formation rate, resulting in net bone loss and osteoporosis. Estrogen is involved in the lipolysis pathway or regulates enzyme expression in glucose and lipid metabolism [6,7]. Estrogen loss significantly increases abdominal fat distribution, lipid accumulation in the adipose tissue, and stimulation of adipocyte differentiation [8,9], possibly related to increased weight gain and metabolic diseases induced by menopausal obesity [10,11].
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