PurposeOsteoarthritis (OA) is an age-related joint disease that is characterised by the degeneration of articular chondrocytes. Ginsenosides, the most important pharmacological ingredients of ginseng, have been proven to provide effective therapy for neurodegenerative diseases and can inhibit cell apoptosis. We investigated whether ginsenoside Rb1 can modulate inflammation and apoptosis in human chondrocytes.MethodsChondrocytes were isolated from OA patients undergoing total knee replacement surgery. Apoptosis was assessed by TUNEL (terminal deoxyribonucleotide transferasemediated dUTP nick end-labelling)-positive staining. Levels of PGE2 and NO2- were detected by ELISA. Gene expression levels were measured for type II collagen (Col2A1), aggrecan, MMP-13, COX-2, iNOS, caspase-3, and PARP.ResultsThe results showed that TUNEL-positive staining chondrocytes were decreased by Rb1 compared with IL-1β. Both 10 or 100 μg/ml Rb1 inhibited the effect of IL-1β on chondrocytes by decreasing levels of PGE2, NO2-, MMP-13, COX-2, iNOS, caspase-3 and PARP and increasing aggrecan and Col2A1 gene expression levels, to block IL-1β-induced cell inflammation and apoptosis.ConclusionsThe results suggest that Rb1 possesses potential anti-inflammatory and anti-apoptotic properties in human chondrocytes, possibly by binding to oestrogen receptors to exert its pharmacological effects.

The mini-subvastus approach could offer faster recovery, less pain and shorter hospital stays without compromising the principles of proper prosthesis position and limb alignment compared with the medial parapatellar approach.

This study aimed to assess whether Ginsenoside Rg1 (Rg1) inhibits inflammatory responses in human chondrocytes and reduces articular cartilage damage in a rat model of osteoarthritis (OA). Gene expression and protein levels of type II collagen, aggrecan, matrix metalloproteinase (MMP)-13 and cyclooxygenase-2 (COX-2) were determined in vitro by quantitative real-time-polymerase chain reaction and Western blotting. Prostaglandin E2 (PGE2) amounts in the culture medium were determined by enzyme-linked immunosorbent assay (ELISA). For in vivo assessment, a rat model of OA was generated by anterior cruciate ligament transection (ACLT). Four weeks after ACLT, Rg1 (30 or 60 mg/kg) or saline was administered by gavage once a day for eight consecutive weeks. Joint damage was analyzed by histology and immunohistochemistry. Ginsenoside Rg1 inhibited Interleukin (IL)-1β-induced chondrocyte gene and protein expressions of MMP-13, COX-2 and PGE2, and prevented type II collagen and aggrecan degradation, in a dose-dependent manner. Administration of Ginsenoside Rg1 to OA rats attenuated cartilage degeneration, and reduced type II collagen loss and MMP-13 levels. These findings demonstrated that Ginsenoside Rg1 can inhibit inflammatory responses in human chondrocytes in vitro and reduce articular cartilage damage in vivo, confirming the potential therapeutic value of Ginsenoside Rg1 in OA.

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Low frequency pulsed electromagnetic field (LFPEMF) has been shown to provide anti-inflammatory and antioxidative effects. However, there are no reports on whether LFPEMF can treat spinal cord injury (SCI) and its therapeutic mechanism. Therefore, this study was conducted to investigate whether LFPEMF can promote the recovery of neurological function after SCI in rats and its therapeutic mechanism. Basso-Beattie-Bresnahan (BBB) score and transcranial magnetic motor-evoked potentials (tcMMEPs) were recorded to assess the recovery of neurological function. Hematoxylin and eosin (HE) staining and luxol fast blue (LFB) staining were performed to assess the severity of SCI. Immunofluorescence (IF) staining and western blotting (WB) were performed to assess the differentiation of oligodendrocyte precursor cells (OPCs) into oligodendrocytes (OLs). Toluidine blue (TB) staining was performed to assess remyelination. WB and enzyme-linked immunosorbent assays (ELISA) were performed to assess the expression of neurotrophins and inflammatory factors. Our results showed that following stimulation by LFPEMF, there were significant improvements in BBB scores, tcMMEP amplitudes, the extent of the damage, and reduced demyelination in rats after SCI. The mature OLs, the number of well-myelinated fibers, and the myelin sheath thickness significantly increased in rats stimulated by LFPEMF after SCI. The expression of neurotrophins significantly increased, and the expression of inflammatory factors significantly decreased in rats stimulated by LFPEMF after SCI. Therefore, we suggest that LFPEMF can promote the recovery of neurological function in rats after SCI by improving the differentiation of OPCs into OLs and promoting remyelination, as well as by inhibiting inflammation and promoting neurotrophic effects. ß

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