Provided that the ERRC a synaptic 5-alpha-reductase protein constitutively active receptor, which is the case for nuclear NDRC. Although the ERRC is highly expressed in the adult rat brain, the position of the ERRC had not been completely in the hippocampus Ndig detected. We have shown clearly that the ERRC in pyramidal cells and K rnerzellen Expressed in the hippocampus, judging by immunostaining Staining and Western blot analysis. Can phosphorylate CREB since ERRC, k Nnte nanomolar BPA also modify gene expression VER. Further studies are important in order light on the signal line, wherein the modulation of synaptic plasticity T CERD to Vergie S. Taking ginseng. Rh1 is becoming increasingly popular because of its leistungsf HIGEN pharmacological activity attracted, but not yet been reported to exhibit anti-cancer activity of t. Rh1 has been shown that anti-allergic and anti-inflammatory activity of t in both M Nozzles and lipopolysaccharide stimulated microglia display. In addition, increased It ht memory and hippocampal excitability and inhibits atopic dermatitis, as Hautl Lesions in hairless Mice. In addition, RH1 acts as estrogen-receptor signaling, the phyto- Activated estrogen. Recently we have shown that has the anti-inflammatory Rh1, such as the inhibition of invasion and migration of monocytes THP first Thus, we investigated the anti-metastatic Rh1 in HepG2 cells. Functional validation was evaluated by carrying out the inhibitory effects of Rh1 in the invasion and migration of HepG2 cells. The molecular mechanisms to assess the anti-metastatic Rh1 was matrix metalloproteinase 1 expression by RT-PCR analysis and immunoblotting and activity t of MMP 1 promoter was measured. We also examined the R Inhibitors Rh1 to an AP  sites 3 and  600 NT in the MMP 1 promoter region on treatment with phorbol myristate acetate in the presence or absence of Rh1. Based on these studies, we provide an experimental basis for the development of Rh1 for use as a therapeutic anti-cancer activity of t against metastatic and in the treatment of hepatocellular Ren cancer. Second Materials and methods 2.1. Rh1 materials were purchased from Ambo Institute. Dulbecco’s modified Eagle’s medium and f Tales serum fromPAA Laboratories were acquired. Matrigel was obtained from BD Biosciences. SP600125 and phorbol myristate acetate were from Sigma Aldrich pyridine, 1H-imidazole SB203580 2 4-yl] and PD98059 4H 1 benzopyran 4, fromCalbiochem purchased. Antique Body or antique Body against phosphor-ERK1 / 2, JNK and p38 MAPK were purchased from Cell Signaling Technology, and an antique Body against AP 1-subunit from Santa Cruz Biotechnology. Chemiluminescence kit was purchased from Amersham Life Sciences. 2.2. Analysis of the ability Lebensf Of the cells of HepG2 cells were grown in DMEM, erg complements With 10% FBS, 100 U / ml penicillin and 100 g / ml streptomycin at 37 in a humidified atmosphere of 5% CO re second The cells were seeded in bo t Their culture and maintained in a tissue culture incubator. Rh1 was dissolved in methanol St and sterilized by filtration through a 0.2 m filter disc. Suitable amounts of Rh1 obtained Stamml Solution was added specified in the culture medium at a final concentration. The cells were then given for the ZEITR Ume incubated. The proliferation of adh Pensions cells was determined by a colorimetric assay using.