Zhirong Wang

osteoclast differentiation, hydroxyapatite resorption activity, and expression of osteoclastogenesis-related genes, such as NFATc1, MMP9, CTSK, Acp5 and c-Fos, in RANKL-induced bone marrow macrophages (BMMs) and RAW264.7 cells. It also reduced intracellular ROS levels by suppressing expression of TRAF6 and NADPH oxidase 1 (NOX1) and increasing expression of antioxidant enzymes such as heme oxygenase-1 (HO-1). Puerarin inhibited TRAF6/ROS-dependent activation of the MAPK and NF-κB signaling pathways in RANKL-induced RAW264.7 cells, and these effects were partially reversed by HO-1 silencing or TRAF6 overexpression. These findings suggest puerarin alleviates loss of bone mass in the OVX-model mice by suppressing osteoclastogenesis via inhibition of the TRAF6/ROS-dependent MAPK/NF-κB signaling pathway.

Patients with Crohn's disease (CD) or ulcerative colitis (UC) undergo various therapies, including antibiotic therapy. This meta-analysis of controlled clinical trials was conducted to evaluate whether the use of antibacterial therapy improves the clinical symptoms of inflammatory bowel disease (IBD). The Medline and Scopus databases were searched and a systematic review was performed. Randomized, controlled trials in which antibiotic therapy was compared with placebo were investigated. A total of 10 randomized, placebo-controlled clinical trials for CD were included in the meta-analysis. The pooling of the data from these trials yielded an odds ratio (OR) of 1.35 [95% confidence interval (CI), 1.16-1.58] for antibiotic therapy compared with placebo in patients with CD. Furthermore, nine randomized placebo-controlled clinical trials for UC matched our criteria and were included in the analysis. The pooling of the data from these trials yielded an OR of 2.17 (95% CI, 1.54-3.05) in favor of antibiotic therapy. These results suggest that antibiotics improve clinical outcomes in patients with IBD.

The phytochemical resveratrol has been reported to induce NQO1, an enzyme involved in detoxification reactions, by as yet undetermined mechanisms. Using K562 cells as a model, we showed that 25-50 microM resveratrol increased NQO1 that peaked at 24-48 h. A 2.5-fold rise in NQO1 protein levels was accompanied by a comparable elevation in mRNA copy number and a 3- to 5-fold increase in NQO1 enzymatic activity. Fluorescent microscopic analysis in combination with transfection experiments with plasmids harboring different segments of the 5'-flanking region of NQO1 gene linked to a reporter provided evidence that the modulation of NQO1 gene expression by resveratrol involved the antioxidant response element ARE, accompanied by an increase in the state of phosphorylation of transcription factor Nrf2 and its re-distribution to the nucleus. This change in cellular localization of Nrf2 may be linked to resveratrol-elicited disruption of the Nrf2-Keapl complex in the cytosol, followed by the translocation of Nrf2 to the nucleus where it locates the ARE-containing 5'-promoter region of NQO1 leading to its transcriptional activation.