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Aging (Albany NY). 2018 Dec 23;10(12):4152-4165. doi: 10.18632/aging.101713.

Mechanistic insight into hyaluronic acid and platelet-rich plasma-mediated anti-inflammatory and anti-apoptotic activities in osteoarthritic mice.

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School of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan.
Division of Allergy, Immunology and Rheumatology, Department of Internal Medicine, Taipei Medical University Hospital, Taipei, Taiwan.
Graduate Institute of Biomedical Materials and Tissue Engineering, College of Biomedical Engineering, Taipei Medical University, Taipei, Taiwan.
Ceramics and Biomaterials Research Group, Advanced Institute of Materials Science, Ton Duc Thang University, Ho Chi Minh City, Vietnam.
Faculty of Applied Sciences, Ton Duc Thang University, Ho Chi Minh City, Vietnam.
School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Department of Neurosurgery, Taipei Medical University Hospital, Taipei, Taiwan.
Stem Cells Center, Van Hanh General Hospital, Ho Chi Minh City, Vietnam.
Stem Cell Research Center, College of Oral Medicine, , Taiwan.
Graduate Institute of Basic Medicine, Fu Jen Catholic University, Taipei, Taiwan.


Osteoarthritis (OA) poses a major clinical challenges owing to limited regenerative ability of diseased or traumatized chondrocytes in articular cartilage. Previous studies have determined the individual therapeutic efficacies of hyaluronic acid (HA) and platelet-rich plasma (PRP) on OA; however, the underlying mechanism is still lacking. Therefore, we investigated mechanistic approach of HA+PRP therapy on chondrocyte apoptosis in IL-1β+TNF-α (I+T) treated in vitro OA model, in addition to in vivo anterior cruciate ligament transection-OA mice model. MTT assay showed an enhanced chondrocyte proliferation and viability in HA+PRP-treated group, compared to I+T, I+T/HA, I+T/PRP, I+T/HA+PRP groups. Further, HA+PRP also significantly suppressed ROS, apoptotic cleaved caspase-3 and PARP, p53 and p21 and MMP-1; whereas, cell cycle modulatory proteins including p-ERK, cyclin B1, D1, and E2 were upregulated. The sub-G1 population and TUNEL assay confirmed the higher abundance of healthy chondrocytes in HA+PRP group. A significantly decreased ARS staining in HA+PRP group was also noted, indicating reduced cartilaginous matrix mineralization compared to other groups. Conclusively, compared to HA or PRP, the combined HA+PRP might be a promising therapy for articular cartilage regeneration in osteoarthritic pathology, possibly via augmented anti-inflammatory, anti-oxidative chondrocyte proliferation and inhibited MMP-1 activity and matrix calcification.


apoptosis; chondrocyte; hyaluronic acid; inflammation; osteoarthritis; platelet-rich plasma

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