Abstract
In Asia, Amomum tsao-ko has long been used as a spice or seasoning in food to stimulate digestion. In the present study, we evaluated the effects of ethanol extract of Amomum tsao-ko (EEAT) on menopausal osteoporosis and obesity. After the administration of EEAT in ovariectomy (OVX) mice models for five weeks, microcomputed tomography and a histological analysis were performed to assess, respectively, the trabecular structure and the fat accumulation in adipose, liver, and bone tissues. We also examined the effects of EEAT on a bone marrow macrophage model of osteoclastogenesis by in vitro stimulation from the receptor activator of nuclear factor-kappa Β ligand (RANKL) through real-time PCR and Western blot analysis. In addition, ultrahigh performance liquid chromatography–tandem mass spectrometry (UHPLC–MS/MS) with authentic standards was applied to characterize the phytochemical profiling of EEAT. We found that EEAT significantly decreased OVX-induced body weight gain and fat accumulation, significantly prevented OVX-induced deterioration of bone mineral density and microstructure of trabecular tissues, and significantly inhibited osteoclast differentiation by downregulating NF-κB/Fos/NFATc1 signaling in osteoclasts. Furthermore, UHPLC–MS/MS identified eight beneficial phytochemicals in EEAT. Collectively, these results suggest that EEAT might be an effective nutraceutical candidate to attenuate menopausal osteoporosis by inhibiting osteoclastogenesis and to prevent obesity by suppressing fat accumulation.
Highlights
Menopause is the natural cessation of menstruation due to the loss of ovarian function
receptor activator of nuclear factor-kappa B ligand (RANKL) or RANK induces the phenotypical change of monocyte precursor cells into multinuclear osteoclasts, representing high levels of tartrate-resistant acid phosphatase (TRAP) activity and staining
The inhibitory effect of ethanol extract of Amomum tsao-ko (EEAT) on osteoclastogenesis through RANKL-induced NF-κB/Fos/nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) pathway appears to play a crucial role in preventing OVX-induced bone loss
Summary
Menopause is the natural cessation of menstruation due to the loss of ovarian function It is accompanied by a high prevalence of severe physiological complications, including osteoporosis and obesity, two factors which have led to considerable clinical and public interest in the subject [1,2]. Estrogen regulates bone homeostasis by suppressing osteoclastic bone resorption and supporting osteoblast and osteocyte bone formation. Hormone treatment in animal ovariectomy (OVX) models or menopausal women by estradiol injection or supplementation of estrogen nutraceuticals restores bone turnover by inhibiting bone resorption while maintaining bone formation [3,4,5]. It has been reported that estrogen loss could increase glucose intolerance, insulin resistance, and fat redistribution to the intra-abdominal area, all of which lead to metabolic complications associated with obesity in women [8,9]
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