Abstract
Background: Adenine is a purine with a role in cellular respiration and protein synthesis. It is considered for its pharmacological potential. We investigated whether anti-inflammatory effect of adenine benefits on the proliferation and maturation of osteoblastic cells. Methods: Human osteoblast-like cells (MG-63) were cultured with adenine under control conditions or pre-treated with 10ng/mL of tumor necrosis factor-α (TNF-α) followed by adenine treatment. Cell viability was examined using dimethylthiazol diphenyltetrazolium bromide (MTT) assay. Expression of cytokines and osteogenic markers were analyzed using quantitative PCR (qPCR) and ELISA. Enzyme activity of alkaline phosphatase (ALP) and collagen content were measured. Results: TNF-α exposure led to a decreased viability of osteoblastic cells. Treatment with adenine suppressed TNF-α-induced elevation in IL-6 expression and nitrite oxide production in MG-63 cells. Adenine induced the osteoblast differentiation with increased transcript levels of collage and increased ALP enzyme activity. Conclusions: Adenine exerts anti-inflammatory activity in an inflammatory cell model. Adenine benefits osteoblast differentiation in normal and inflammatory experimental settings. Adenine has a potential for the use to treat inflammatory bone condition such as osteoporosis.
Highlights
Adenine is a purine with a role in cellular respiration and protein synthesis.It is considered for its pharmacological potential
The results showed that adenine had no cytotoxicity on the of MG-63 cells (Figure 1A)
We studied the anti-inflammatory activity of adenine with emphasis on the proliferation differentiation of osteoblast
Summary
Adenine is a purine with a role in cellular respiration and protein synthesis.It is considered for its pharmacological potential. Adenine is a purine with a role in cellular respiration and protein synthesis. We investigated whether anti-inflammatory effect of adenine benefits on the proliferation and maturation of osteoblastic cells. Osteoporosis is a common bone disease, which is characterized by poor bone strength and bone loss It contributes to bone fragility and in turn fracture. Osteoporosis affects an estimated 75 million people in Europe, USA and Japan and causes more than approximately 9 million fractures worldwide every year [1,2]. It is prevalent in postmenopausal women, attributable to estrogen deficiency-related imbalanced bone resorption. Pro-inflammatory cytokines, such as primarily TNF-α and interleukin (IL)-6, are known to contribute to bone resorption and impaired bone remodeling, leading to deteriorated
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