Abstract
Platelet Rich Plasma Regulates Wnt/Beta-Catenin Signal Pathway in Rabbit Chondrocytes by Mediating Interleukin 1 Beta
Department of Anesthesiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, 1Department of Pain Management, The Affiliated Huai’an Hospital of Xuzhou Medical University and The Second People’s Hospital of Huai’an, Huai’an, 223002, 2Department of Interventional Radiology, The Affiliated Huai’an Hospital of Xuzhou Medical University and The Second People’s Hospital of Huai’an, Huai’an, 223002, 3Department of Neurosurgery, The Affiliated Huai’an Hospital of Xuzhou Medical University and The Second People’s Hospital of Huai’an, Huai’an, 223002, 4Department of Anesthesiology, The Affiliated Huai’an Hospital of Xuzhou Medical University and The Second People’s Hospital of Huai’an, Huai’an, 223002, China
Correspondence Address:
Q. X. ZHANG, Department of Pain Management, The Affiliated Huai’an Hospital of Xuzhou Medical University and The Second People’s Hospital of Huai’an, Huai’an, 223002, China, E-mail: qianxizhan_cn@163.com
It was reported that platelet rich plasma can reduce the degeneration of articular cartilage. The purpose of this study was to investigate the effect of platelet rich plasma on Wnt/beta-catenin signal transduction in rabbit chondrocytes. Platelet rich plasma was prepared from the ear vein blood of 3-mo old New Zealand white rabbits. Chondrocytes were isolated from knee cartilage and cultured. The cell identification and the effect of platelet rich plasma on the viability of chondrocytes were measured by the C-terminal telopeptide II and proteoglycan staining. Chondrocytes were divided into 5 groups, control group, interleukin-1 beta group, platelet rich plasma (100 x dilutions) group, Dickkopf WNT signaling pathway inhibitor 1 (100 ng/mL) group and Dickkopf WNT signaling pathway inhibitor 1+platelet rich plasma group. After being treated with interleukin-1 beta (50 μL, 10 μg/mL) for 24 h, the morphology of chondrocytes was observed by an electron microscope. The levels of C-terminal telopeptide II and cartilage oligomeric matrix protein in the culture medium were determined by enzyme linked immunosorbent assay. The messenger RNA and protein expression levels of Wnt-1, beta-catenin and glycogen synthase kinase 3 beta were detected by Real-time polymerase chain reaction and Western blot respectively. Platelet rich plasma promotes the proliferation of chondrocytes. The chondrocytes in the interleukin-1 beta group showed an ultrastructural abnormality, which was not obvious in platelet rich plasma group, Dickkopf WNT signaling pathway inhibitor 1group, and Dickkopf WNT signaling pathway inhibitor 1+platelet rich plasma group. The concentrations of C-terminal telopeptide II and cartilage oligomeric matrix protein in the interleukin-1 beta group were higher than those in the control group, platelet rich plasma group, Dickkopf WNT signaling pathway inhibitor 1group and Dickkopf WNT signaling pathway inhibitor 1+platelet rich plasma group. Compared with the control group, platelet rich plasma group, Dickkopf WNT signaling pathway inhibitor 1group and Dickkopf WNT signaling pathway inhibitor 1+platelet rich plasma group, the expression of Wnt1 and beta-catenin was higher and the level of glycogen synthase kinase 3 beta was lower in the interleukin-1 beta group. Platelet rich plasma may protect interleukin-1 beta activated chondrocytes by inhibiting Wnt/beta-catenin signal.
