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Taraxasterol protects osteoblasts from high glucose by regulating ERK 1/2

Yu Zhang^a,b, Ramizu Bin Shaari^a,*, Mohamad Arif Bin Awang Nawi^a, Akram Bin Hassana, Caiyun Cui^c

 
ABSTRACT:     Chronic hyperglycemia in diabetic patients adversely affects osteoblast distribution, potentially leading to inflammation and cellular damage. Diabetic osteoporosis develops in part due to oxidative damage caused by high glucose (HG) levels. Taraxasterol has anti-inflammatory, anti-oxidative, and anti-tumor properties; it is derived from the Compositae plant Taraxacum. Preliminary research indicates taraxasterol potential to enhance osteoblast proliferation and differentiation, yet its protective properties in high-glucose conditions are not well-documented. We established a taraxasterol concentration of 10 ?g/ml based on cell toxicity assays. Cell proliferation, alkaline phosphatase (ALP) activity, oxidative stress (OS) levels, and mRNA expression of osteogenic genes like Runt-related transcription factor 2 (Runx2) and ALP were measured in the study to determine the effect of taraxasterol on the MC3T3-E1 cell line in HG conditions. To assess the levels of phosphorylated ERK (p-ERK) and extracellular signal-regulated kinase (ERK), Western blot analyses were performed. The results showed taraxasterol highly expressed osteogenic markers such as ALP and Runx2 in the presence of HG, decreased OS, and accelerated the proliferation and differentiation of MC3T3-E1 under the HG condition. More importantly, it reduced the activation of the ERK pathway systematically activated by the presence of HG. Therefore, our study suggests that taraxasterol can mitigate OS and enhance the proliferation and differentiation of osteoblasts in HG environments. This effect may be associated with taraxasterol ability to inhibit the upregulation of ERK and p-ERK expression induced by HG.

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* Corresponding author, E-mail: ramizu@usm.my

Received 3 Feb 2024, Accepted 20 Jul 2024