article · Antioxidants
Glucocorticoid use, such as dexamethasone, is a leading secondary cause of osteoporosis. Researchers investigated whether an aqueous chicory extract and an ethanolic purslane extract could prevent dexamethasone-induced osteoporosis in rats, comparing their performance to the standard drug alendronate. Dexamethasone caused bone degradation by driving oxidative stress, reducing protective bone growth markers, and elevating markers associated with bone turnover and resorption. When administered individually or in combination, the chicory and purslane extracts exhibited clear protective effects against these bone-depleting actions. The treatments modulated key molecular signalling networks, specifically the Nrf2/HO-1 antioxidant pathway and the RANK/RANKL/OPG pathway, while also preserving healthy histopathological bone architecture. The combined extract demonstrated a strong synergistic effect that mitigates bone loss through biological mechanisms distinct from those of alendronate.
Long-term steroid treatments are essential for many illnesses, but they frequently lead to severe bone loss and fractures. Finding alternative, plant-derived therapies could offer new strategies to prevent or manage this common side effect, potentially providing safer protective options with different biological actions compared to current pharmaceutical standards.
This research could inform the development of botanical dietary supplements or complementary therapeutics for patients undergoing long-term steroid therapy. Potential users would include pharmaceutical or nutraceutical companies formulating bone health products. Because the findings are based exclusively on in vivo rat studies, the application remains at an early, preclinical stage requiring clinical validation.
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The prolonged use of exogenous glucocorticoids, such as dexamethasone (Dex), is the most prevalent secondary cause of osteoporosis, known as glucocorticoid-induced osteoporosis (GIO). The current study examined the preventative and synergistic effect of aqueous chicory extract (ACE) and ethanolic purslane extract (EPE) on GIO compared with Alendronate (ALN). The phytochemical contents, elemental analysis, antioxidant scavenging activity, and ACE and EPE combination index were evaluated. Rats were randomly divided into control, ACE, EPE, and ACE/EPE MIX groups (100 mg/kg orally), Dex group (received 1.5 mg Dex/kg, Sc), and four treated groups received ACE, EPE, ACE/EPE MIX, and ALN with Dex. The bone mineral density and content, bone index, growth, turnover, and oxidative stress were measured. The molecular analysis of RANK/RANKL/OPG and Nrf2/HO-1 pathways were also evaluated. Dex causes osteoporosis by increasing oxidative stress, decreasing antioxidant markers, reducing bone growth markers (OPG and OCN), and increasing bone turnover and resorption markers (NFATc1, RANKL, ACP, ALP, IL-6, and TNF-α). In contrast, ACE, EPE, and ACE/EPE MIX showed a prophylactic effect against Dex-induced osteoporosis by modulating the measured parameters and the histopathological architecture. In conclusion, ACE/EPE MIX exerts a powerful synergistic effect against GIO by a mode of action different from ALN.
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DOI: 10.3390/antiox13010066
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