Ter, the decreased IkB steadily recovered (Figure 5A and B). These outcomes recommend that H. pylori can cause IkB degradation. Based on this, we observed the effects of RCderived diterpenoid C on IkB degradation triggered by H. pylori, and foud that IkB was basically unchanged. This suggests that RGderived diterpenoid C can inhibit IkB degradation caused by H. pylori (Figure 5C). Expression of IkB and p65 phosphorylated proteins, and I B kinase , I B kinase and p65 proteins H. pylori swiftly induced phosphorylation of p65 and IkB proteins. p65 phosphorylation was clearly seen at five min time point, and was by far the most powerful in between 15 and 30 min, and then steadily weakened. IkB phosphorylation was observed at five min time point, and was themost strong at 15 min time point, and then gradually weakened. In a brief time, the expression of p65, IB kinase (IKK) and IKK proteins was not markedly changed in H. pylori group. These results suggest that H. pylori is really a very good activator of NFB signal pathways. RCderived diterpenoid C inhibited H. pyloriinduced p65 and IkB phosphorylation, decreased the expression of p65, IKK and IKK proteins (Figure 6). These benefits indicated that RCderived diterpenoid C decreased IkB protein degradation via inhibiting phosphorylation of p65 and IkB plus the expression of IKK and IKK proteins. RCderived diterpenoid C may be an effective inhibitor of NFB.DISCUSSIONRecent studies indicate that H. pylori activates NFB by means of two pathways. A single pathway is dependent on CagWJG|www.wjgnet.comAugust 21, 2013|Volume 19|Issue 31|Huang X et al . Effects of radix curcumaederived diterpenoid CALevel of IL8 ten (pg/mL)three.5 three 2.5 2 1.5 1 0.5Blank group Model group Lowconcentration diterpenoid C group Moderateconcentration diterpenoid C group Highconcentration diterpenoid C group Amoxicillin group24 48 Time right after treatment (h)B90 80Blank group Model group Lowconcentration diterpenoid C group Moderateconcentration diterpenoid C group Highconcentration diterpenoid C group Amoxicillin groupLevel of IL4 (pg/mL)60 50 40 30 20 ten 0 12 24 48 Time after remedy (h)Figure 3 Effects of radix curcumaederived diterpenoid C on Helicobacter pyloriinduced human gastric epithelium cell line cell inflammation.1-Aminobenzotriazole Chemical name A: The alterations in the degree of interleukin (IL)8 in cell supernatant; B: The changes within the amount of IL4 in cell supernatant.1823257-80-2 Data Sheet H.PMID:24818938 pylori Diterpenoid C H. pylori p65 (nucleus) p65 (cytosol)AIkB actinHelicobacter pylori90 minactinBIkBHelicobacter pylori30 minFigure 4 Effects of radix curcumaederived diterpenoid C on nucleic localization of nuclear element kappa B p65. H. pylori: Helicobacter pylori.actinpathogenicity island (CagPAI), but independent of CD14 and interleukin1 receptorassociated kinase. Another pathway is dependent on CD14 and tolllike receptor 4, but independent of CagPAI. H. pylori chiefly activates NFB classics method. So it is actually crucial to p53 moving nuclear and IkB degradation in NFB classics method. Additionally, H. pylori infection induces IkB attenuation. In gastric cancer cells, the activities of IkB and IkB are boost, and the phosphorylation of serine residues of IkB and IkB induces the degradation of regulatory proteins of NFB, activating NFB. H. pylori infection could induce gastric mucosal inflammatory, and improve the release of PGE2, IL8 and ROS[1012], the possible mechanism of which may be connected to NFB pathways[13].CIkB actinDiterpenoid C Helicobacter pylori 530 minFigure five Effects of radix curcumaederived diterp.
