The abnormal maturation and ossification of articular chondrocytes play a central role in the pathogenesis of osteoarthritis (OA). Inhibiting the enzymatic degradation of the extracellular matrix and maintaining the cellular phenotype are two of the major goals of interest in managing OA. Ginseng is frequently taken orally, as a crude substance, as a traditional medicine in Asian countries. Ginsenoside Rb1, a major component of ginseng that contains an aglycone with a dammarane skeleton, has been reported to exhibit various biological activities, including anti-inflammatory and anti-tumor effects. However, a chondroprotective effect of ginsenoside Rb1 related to OA has not yet been reported. The purpose of this study was to demonstrate the chondroprotective effect of ginsenoside Rb1 on the regulation of pro-inflammatory factors and chondrogenic genes. Cultured rat articular chondrocytes were treated with 100 μM ginsenoside Rb1 and/or 500 μM hydrogen peroxide (H2O2) and assessed for viability, reactive oxygen species production, nitric oxide (NO) release, and chondrogenic gene expression. Ginsenoside Rb1 treatment resulted in reductions in the levels of pro-inflammatory cytokine and NO in H2O2-treated chondrocytes. The expression levels of chondrogenic genes, such as type II collagen and SOX9, were increased in the presence of ginsenoside Rb1, whereas the expression levels of inflammatory genes related to chondrocytes, such as MMP1 and MMP13, were reduced by approximately 50%. These results suggest that ginsenoside Rb1 has potential for use as a therapeutic agent in OA patients.
To elucidate the effects of heme oxygenase-1 (HO-1) on a neurotoxic substance, 1-methyl-4-phenylpyridinium (MPP + ), induced cytotoxicity in immune cells, cell death, and the production of reactive oxygen species (ROS) were studied using Raw 264.7 macrophages. HO-1 is induced by harmful stimuli including oxidative stress, and it exerts a protective effect against cytotoxicity in immune cells. Using Western blotting analysis, we have evaluated the expression of HO-1 in Raw 264.7 macrophages treated with MPP + . Via a WST assay and flow cytometric analysis, we have also evaluated the cytoprotective effect of HO-1 induction against the cytotoxicity induced by exposure to MPP + . In Raw 264.7 macrophage exposed MPP + cells, HO-1 expression evidenced a rapid increase, peaking at 12 h. The increment of cell death and ROS production due to MPP + exposure were aggravated further by treatment with Tin protoporphyrin-IX (SnPP-IX, HO-1 inhibitor). The increased cell death and ROS production induced by MPP + exposure were recovered to a significant degree by treatment with Cobalt protoporphyrin-IX (CoPP-IX, HO-inducer). According to these results, HO-1 induction exerts a cytoprotective effect on MPP + -induced cytotoxicity, which is related to ROS production.
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