Abstract

BackgroundSHINBARO is a refined herbal formulation used to treat inflamed lesions and bone diseases. This study aimed to investigate the anti-osteoarthritic activities of intra-articular administration of SHINBARO and determine its underlying molecular mechanism in a monosodium iodoacetate (MIA)-induced osteoarthritis rat model.MethodsMale Sprague–Dawley rats received a single intra-articular injection of MIA into the infrapatellar ligament of the right knee. Subsequently, the rats were treated with normal saline, SHINBARO, and diclofenac once daily for 21 days. Rats treated with normal saline, but not MIA, comprised the control group. Histological changes in the femur of the MIA-induced osteoarthritis rat model were observed by micro-computed tomography scanning and staining with hematoxylin and eosin, and safranin-O fast green. Serum levels of PGE2 and anti-type II collagen antibodies in the MIA-induced osteoarthritis rat model were measured using commercial kits. Protein levels of inflammatory enzymes (iNOS, COX-2), pro-inflammatory cytokines (TNF-α, IL-1β), and inflammatory mediators (NF-κB, IκB) in cartilaginous tissues were determined by western blot analysis.ResultsIntra-articular administration of SHINBARO (IAS) at 20 mg/kg remarkably restrained the decrease in bone volume/total volume, being 28 % (P = 0.0001) higher than that in the vehicle-treated MIA group. IAS (2, 10, and 20 mg/kg) treatment significantly recovered the mean number of objects values with increased percentage changes of 13.5 % (P = 0.147), 27.5 % (P = 0.028), and 44.5 % (P = 0.031), respectively, compared with the vehicle-treated MIA group. The serum level of PGE2 in the IAS group at 20 mg/kg was markedly inhibited by 60.6 % (P = 0.0007) compared with the vehicle-treated MIA group, and the anti-collagen type II antibody level in the IAS group was reduced in a dose-dependent manner. IAS (20 mg/kg) effectively suppressed the induction of inflammation-mediated enzymes (iNOS and COX-2) and pro-inflammatory cytokines (TNF-α and IL-1β). IAS treatment also downregulated the NF-κB level and increased the IκB-α level in the MIA- induced osteoarthritis rat model.ConclusionSHINBARO inhibited PGE2 and anti-type II collagen antibody production and modulated the balance of inflammatory enzymes, mediators, and cytokines in the MIA-induced osteoarthritis rat model.Electronic supplementary materialThe online version of this article (doi:10.1186/s13020-016-0089-6) contains supplementary material, which is available to authorized users.

Highlights

  • SHINBARO is a refined herbal formulation used to treat inflamed lesions and bone diseases

  • This study aimed to investigate the anti-osteoarthritic activities of intra-articular administration of SHINBARO and determine its underlying molecular mechanism in an monosodium iodoacetate (MIA)-induced OA rat model

  • The Intra-articular administration of SHINBARO (IAS) group, oral SHINBARO (OS) group, and diclofenac group did not show any significant differences compared with the vehicle-treated MIA groups

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Summary

Introduction

SHINBARO is a refined herbal formulation used to treat inflamed lesions and bone diseases. This study aimed to investigate the anti-osteoarthritic activities of intra-articular administration of SHINBARO and determine its underlying molecular mechanism in a monosodium iodoacetate (MIA)-induced osteoarthritis rat model. Osteoarthritis (OA) is a degenerative joint disease characterized by abrasion of articular cartilage and trabecular. Monosodium iodoacetate (MIA) is an inhibitor of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) that results in a reduction of glycolysis and causes articular cartilage changes related to the histological and morphological features of OA by impeding integration of the chondral structure and inducing cell death of chondrocytes [15]. MIA causes a repeated progression of synovial hyperplasia and inflammatory cell infiltration, destroys articular cartilage, and induces bone loss and chondral deformation [16]. Injection of MIA into the knee joints of rats is considered a suitable model that resembles the phenomena observed in human OA and is applied for evaluation of chondroprotective activity [17]

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