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Published on: May 21, 2013
Curcumin Promotes Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells from Anterior Cruciate Ligament
Zhaoyong Zeng1,2, Zhiqiang Bao2, Jianping Zhang2
1Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangzhou, 510630, China.
Introduction:
Curcumin and bone marrow-derived mesenchymal stem cells (BMSCs) with osteogenic differentiation potential can promote tendon-bone healing. This study revealed the specific mechanisms by which curcumin promotes osteogenic differentiation of BMSCs.
Materials And Methods:
BMSCs were isolated from mice undergoing anterior cruciate ligament reconstruction (ACLR) or from control mice and subsequently characterized using flow cytometry. CCK-8 and flow cytometry were used to assess the survival and apoptosis of ACLR-modeled BMSCs with or without curcumin treatment, and the osteogenic potential in vitro was evaluated via alkaline phosphatase (ALP) and Alizarin Red S (ARS) staining. The levels of relevant downstream mediators were measured by qRTPCR and immunoblotting. A rescue assay was performed to validate the interplay between curcumin and the extracellular signal-regulated protein kinase (ERK) pathway using the ERK inhibitor U0126.
Results:
The isolated cells were characterized as positive for CD44, CD90, and CD105, and negative for CD45 and CD34, confirming their phenotype as BMSCs. Curcumin intervention promoted the survival and osteogenic potential of CD44+CD90+CD105+ ACLR/ BMSC and inhibited apoptosis in vitro; however, these promoting effects were negated following treatment with ERK inhibitor U0126. Moreover, U0126 reversed the promoting effects of Curcumin on the phosphorylation of ERK1/2 and BAD in vitro.
Discussion:
This study investigated the potential effects of curcumin on the osteogenic differentiation of CD44+CD90+CD105+ ACLR/BMSCs in vitro, providing novel evidence for the therapeutic potential of curcumin in ACLR.
Conclusion:
Curcumin can enhance the osteogenic differentiation potential of CD44+CD90+CD105+ ACLR/BMSCs in vitro via the ERK pathway, thereby promoting tendon-bone healing following ACLR. However, these findings require further experimental validation.
