As the main active constituent of Andrographis paniculata that was applied in treatment of many diseases including inflammation in ancient China, andrographolide (ANDRO) was found to facilitate reduction of edema and analgesia in arthritis. This suggested that ANDRO may be promising anti-inflammatory agent to relieve destruction and degeneration of cartilage after inflammation. In this study, the effect of ANDRO on rabbit articular chondrocytes in vitro was investigated. Results showed that not more than 8 μM ANDRO did no harm to chondrocytes (P < 0.05). DNA content and glycosaminoglycan (GAG) /DNA were, respectively, improved in ANDRO groups comparing to the control (P < 0.05). ANDRO could promote expression of aggrecan, collagen II, and Sox9 genes while downregulating expression of collagen I gene (P < 0.05). Furthermore, hypertrophy that may result in chondrocyte ossification could not be detected in all groups (P > 0.05). The viability assay, hematoxylin-eosin, safranin O, and immunohistochemical staining also showed better performances in ANDRO groups. As to the doses, 3 μM ANDRO showed the best performance. The results indicate that ANDRO can accelerate proliferation of rabbit articular chondrocytes in vitro and meanwhile maintain the phenotype, which may provide valuable references for further exploration on arthritis.

Abstract. Numerous antioxidants exhibit antiarthritic effects due to their inhibitory effect on inflammatory factors. Certain antioxidants, such as protocatechuic acid (PCA) and its analogs, have been reported to be effective in the treatment of arthritis. However, the effect of PCA on chondro-protection may be alleviated due to the induction of apoptosis, as has been demonstrated in stomatocytes. To clearly determine the effect of PCA on the biological and cellular metabolism of rabbit articular chondrocytes in vitro, examinations of cytotoxicity, proliferation and morphology were performed, in addition to analyses of glycosaminoglycan (GAG) synthesis and the expression of cartilage-specific genes. The results revealed that PCA effectively promoted chondrocyte growth, the synthesis of the extracellular matrix and the mRNA expression of aggrecan, collagen II and Sox9, while downregulating the expression of the collagen I gene, a marker of chondrocyte dedifferentiation. In addition, hypertrophy, which may result in chondrocyte ossification, was not detected in the groups. Among the doses (range, 0.05-0.3 mmol/l) of PCA that promoted the proliferation of chondrocytes, a concentration of 0.125 mmol/l produced the optimum performance. The results indicated that PCA, particularly at a dose of 0.125 mmol/l, accelerated the proliferation of rabbit articular chondrocytes in vitro and maintained their phenotype. This study may provide a basis for further research concerning the treatment of cartilage defects.

BackgroundPeridural fibrosis (PF) is a normal complication after lumbar surgery. It is a challenge for both surgeons and patients. Rapamycin (RPM), a novel antibiotic with anti-proliferative and immunosuppressive properties, has been shown to be effective in preventing uncontrolled scar proliferation diseases. The object of the present research was to investigate the effects of RPM on inhibiting PF in vitro and in vivo.Material/MethodsIn vitro, the fibroblasts collected and isolated from the rat tail skin were cultured with/without RPM and cell counting was performed. In vivo, the double-blinded study was conducted in 60 healthy Wistar rats divided randomly into 3 groups: 1) RPM treatment group; 2) Vehicle treatment group; 3) Control group. Rats underwent a L1-L2 level laminectomy with a satisfactory anesthetization. Four weeks post-operatively, the Rydell score, histological analysis, hydroxyproline content, vimentin expressional level, and inflammatory cytokines expressional levels were assessed.ResultsIn vitro, RPM showed ability to prevent fibroblast proliferation. In vivo, the laminectomy was well tolerated by all rats, which were killed 4 weeks post-operatively. The Rydell score, histological evaluation, hydroxyproline content, vimentin expression level, and inflammatory activity showed the positive effect of RPM in preventing peridural adhesion, inhibiting fibrotic formation and collagen synthesis, and down-regulating inflammation.ConclusionsIn the present primary study, RPM showed good efficacy in preventing the proliferation of fibroblasts. RPM can prevent rat peridural adhesion through inhibiting collagen synthesis, fibroblasts proliferation, and inflammatory activity.