Research Paper Volume 10, Issue 12 pp 4152—4165
Mechanistic insight into hyaluronic acid and platelet-rich plasma-mediated anti-inflammatory and anti-apoptotic activities in osteoarthritic mice
- 1 School of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan
- 2 Division of Allergy, Immunology and Rheumatology, Department of Internal Medicine, Taipei Medical University Hospital, Taipei, Taiwan
- 3 Graduate Institute of Biomedical Materials and Tissue Engineering, College of Biomedical Engineering, Taipei Medical University, Taipei, Taiwan
- 4 Ceramics and Biomaterials Research Group, Advanced Institute of Materials Science, Ton Duc Thang University, Ho Chi Minh City, Vietnam
- 5 Faculty of Applied Sciences, Ton Duc Thang University, Ho Chi Minh City, Vietnam
- 6 School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
- 7 Department of Neurosurgery, Taipei Medical University Hospital, Taipei, Taiwan
- 8 School of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan
- 9 Stem Cells Center, Van Hanh General Hospital, Ho Chi Minh City, Vietnam
- 10 Stem Cell Research Center, College of Oral Medicine, , Taiwan
- 11 Graduate Institute of Basic Medicine, Fu Jen Catholic University, Taipei, Taiwan
Received: August 24, 2018 Accepted: December 6, 2018 Published: December 23, 2018
https://doi.org/10.18632/aging.101713How to Cite
Abstract
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.