Rg3 and F4 are unique to Korean Red Ginseng. These results may suggest the importance of Korean Red Ginseng for treating cartilage degradation disorders. In conclusion, some ginsenoside-enriched fractions

(n-BuOH fraction, GDF, and GDF/F4) were, for the first time, found to inhibit MMP-13 expression from chondrocytes, at least in part, via blocking the activation of p38 MAPK, JNK, and STAT-1/2. GDF/F4 also showed some protective activity against cartilage degradation in rabbit cartilage tissue culture. Our study may open a new therapeutic area for red ginseng product(s). These products may be beneficial for chondroprotection in cartilage degradation-related disorders such as osteoarthritis. All authors have no conflict of interest to declare. This study was supported by 2014 Research Grant AZD8055 order from Kangwon National University (No. 120140154) and BK21-plus project from Ministry of Education (Korea, No. F14SR08T4520). A part of this study was also supported by an MRC grant to Y.S. Kim funded by

the National Research Foundation of Korea (No. 2011-0030635). The bioassay facilities of the New Drug Development Institute (Kangwon National University, Chunchon, selleck screening library Korea) were used. “
“The α and β estrogen receptors (ERs) regulate various brain functions in an estradiol-dependent manner. Signaling pathways elicited via ER-α and ER-β activation are interrelated and feedback inhibition

occurs mainly by estradiol engagement of the ER-α receptor. Most studies involving ER-β have focused on brain functions and behavioral patterns [1] and [2]. ER-β is a member of the nuclear receptor superfamily [3]. Upon ligand binding, ER-β regulates gene expression by binding directly to regulatory regions of target genes or by interacting with other transcription factors such as nuclear factor κB, activating until protein 1, and stimulating protein 1 [4]. ER-β also controls gene expression by activating signaling pathways that stimulate kinases such as protein kinase A, protein kinase C, and mitogen-activated protein kinase [5]. Recent studies show that ER-β has neuroprotective, anti-inflammatory, antiproliferative, antioxidant, and immune-modulatory activities [2] and [6]. However, the effects of stress on ER-β expression in the brain cells remain largely unknown. ERs regulate activation of phosphatidylinositol-3 kinases (PI3Ks) by interacting with the p85 regulatory subunit of PI3K [7]. Activation of ER-α upregulates PI3K/Akt signaling, which in turn stimulates cell growth in breast cancer cells [8]. ER-β also activates signaling through PI3K/Akt and improves myocardial function in female hearts following acute ischemia [9].