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Osteoporosis is a major cause of bone fracture in post-menopausal women. We evaluated the effects of pristimerin treatment on ovariectomy-induced osteoporosis, and its possible molecular mechanism.    Material and methods  Rats were ovariectomised and biochemical markers of bone formation were determined from serum samples. The microarchitectures of bone tissues were analyzed via micro-CT scans and Western blotting assays. The cytotoxic effects of pristimerin, the differentiation of osteoclasts, and bone reabsorption were evaluatedin vitrousing RAW 264.7 cells.    Results  Treatment with pristimerin attenuated changes in markers of bone formation and reabsorption such as creatine kinase (CK), alkaline phosphatase (ALP), tartrate-resistant acid phosphatase (TRAP), collagen type I fragments (CTX), bone Gla-protein (BGP), and osteocalcin (OC) in the serum of ovariectomised rats. It also appeared to restore the microarchitecture of bone tissue. The expression levels of TNF receptor-associated factor 6 (TRAF-6), nuclear factor k light chain enhancer of activated B cells (NF-κB p65), and receptor activator of nuclear factor-κB ligand (RANKL) protein were significantly lower, while those of Akt and PI3K were significantly higher, in the bone tissues of the pristimerin-treated group than in negative controls. Pristimerin had no cytotoxic effect on RAW 264.7 cells and reduced the differentiation of osteoclasts, bone reabsorption, and translocation of p65 in RANKL-stimulated RAW 264.7 cellsin vitro    .    Conclusions  Pristimerin reduces the effects of osteoporosis by restoring the altered RANKL/TRAF-6/NF-κB pathway in ovariectomised rats.

Beneficial effect of pristimerin against the development of osteoporosis in ovariectomy-induced osteoporosis rats by the RANKL/TRAF6/NF-κB pathway