Abstract
Cuscuta chinensis Lam. (Convolvulaceae) is an important herbal medicine widely used to improve sexual function, treat osteoporosis, and prevent aging, and has been reported to exhibit anti-osteoporotic effects in vitro. However, the activity of Cuscuta chinensis Lam. on glucocorticoid-induced osteoporosis still remains unclear. The present study aimed to assess the protective effect and the underlying mechanism of action of Cuscuta chinensis extract (CCE) against glucocorticoid-induced osteoporosis in vivo. Sprague-Dawley rats were randomly divided into four groups as follows: control group, osteoporosis group, and 2 CCE-treated osteoporosis groups (100 mg·kg-1·day-1). Blood samples and femur bones were collected for immunohistochemistry, biochemical, mRNA expression, and western blot analysis. HPLC analysis revealed that chlorogenic acid, quercetin, and hyperin were the major constituents of CCE. The results indicated that CCE increased bone length, bone weight, and bone mineral density and suppressed dexamethasone (DEX)-induced reduction in body weight. In addition, TRAP staining indicated that CCE reduced osteoclasts in DEX-induced osteoporosis rats. Mechanistically, CCE treatment alleviated the increase of bone resorption markers and the decline of osteogenic markers, which might be partially mediated by regulation of RANKL/OPG and RunX2 pathways. These results suggest that CCE showed promising effects in the protection against glucocorticoid-induced osteoporosis through protecting osteoblasts and suppressing osteoclastogenesis.
Highlights
Osteoporosis is a systemic metabolic disease, characterized by a decline in bone mass and deterioration of bone microstructure, which results in increased risk of bone fractures and bone fragility, and the main reason for broken bones in the elderly [1]
Sprague-Dawley rats were randomly divided into four groups (n=8) as follows: control group (CON), osteoporosis group (DEX), and 2 groups of rats with osteoporosis receiving 100 mg/kg Cuscuta chinensis extract (CCE) (DEX+CCE); the dose of CCE (100 mg/kg) was based on previous research [19] and our preliminary experiments
The result indicated that CCE suppressed osteoclastic bone resorption in DEX-induced osteoporosis in rats
Summary
Osteoporosis is a systemic metabolic disease, characterized by a decline in bone mass and deterioration of bone microstructure, which results in increased risk of bone fractures and bone fragility, and the main reason for broken bones in the elderly [1]. Osteoporosis occurs due to other diseases such as hyperthyroidism, alcoholism, oophorectomy, and kidney disease [2]. Epidemiologic research has indicated synthetic drugs such as selective serotonin reuptake inhibitors, glucocorticoids, and proton pump inhibitors could lead to the induction of osteoporosis [3]. Glucocorticoids are widely used in the treatment of rheumatic disease, autoimmune disease, and organ transplantation due to their immunosuppressive and antiinflammatory effects [4]. Long-term glucocorticoid therapy is associated with an incidence of osteoporosis, which is one of themost serious side effects of glucocorticoid therapy [5]. It is important to understand the pathogenesis of glucocorticoid-induced osteoporosis and develop a novel therapeutic strategy for prevention and treatment of osteoporosis
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