Abstract
Objective: Eurycoma longifolia (EL), a well-recognized Malaysian medicinal herb, has gained widespread popularity due to its ability to protect against bone calcium loss in androgen-deficient osteoporosis. Nevertheless numerous animal studies have proved the bone protective effect of EL; however, the exact mechanism is not well-explained yet. Thus, the present study was aimed to explore the in vitro basis of bone protective effects of EL by using mouse pre-osteoblast cell line (MC3T3-E1).Methods: The cytotoxicity and proliferative potential of EL were evaluated by lactate dehydrogenase (LDH) and cell counting methods. Despite cell growth, the ability of EL to promote osteogenic differentiation of bone-forming cells was assessed by quantifying collagen (early differentiation marker) and calcium (late differentiation marker) in EL-treated bone forming cells.Results: Resulting data obtained from dose optimization study revealed that EL at 5 to 50 µg/ml concentration showed marked effects in significantly promoting cell growth in MC3T3-E1 cells. As such, resulting data also demonstrated the superior potential of EL in up regulating collagen synthesis and mineralization (calcium deposition) in MC3T3-E1 cells at 25 µg/ml, in comparison to untreated (negative control) and dihydrotestosterone (5α-DHT)-treated cells (positive control).Conclusion: These pronounced effects of EL on osteoblasts provide an in vitro basis for the bone protective potential of EL and thus can be considered as an alternative regimen for the treatment of androgen-deficient male osteoporosis.
Highlights
Osteoporosis is one of the most prevalent bone diseases resulting from an overwhelming imbalance in bone remodeling
The MC3T3-E1 cells treated with Eurycoma longifolia (EL), at lower concentrations (1–50 μg/ml), showed 100% viability; a further increase in the concentration of EL (>50 μg/ml) produced a sign of toxicity towards MC3T3-E1 cells
In conclusion, this study has demonstrated for the first time that EL promoted osteoblasts proliferation, osteoblast differentiation and mineralization of extracellular matrix (ECM)
Summary
Osteoporosis is one of the most prevalent bone diseases resulting from an overwhelming imbalance in bone remodeling. It is characterized by an excessive bone resorption by osteoclasts relative to the bone formation by osteoblasts [1,2,3]. Osteoblasts are primarily regulated by progesterone and testosterone, while osteoclasts require estrogen-like hormones to exert their functional roles. It is well-established that sex hormones (estrogen, progesterone and androgen) are among the crucial modulators of bone health, in protecting bones from weakness and regulating bone minerals to optimum levels [5,6,7]. The unbalanced cellular activity which could result in the intermittent bone formation and resorption is most commonly associated with the development of metabolic bone disorders (including osteoporosis) and related bone fractures [2, 11]
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