Oxyresveratrol Is a Phytoestrogen Exerting Anti-inflammatory Effects Through NF-κB and Estrogen Receptor Signaling.

Recent studies suggest an anti-inflammatory activity of oxyresveratrol, a stilbene extracted from Cortex mori root used in traditional Chinese medicine that also presents estrogen-like activity. We herein tested the hypothesis that oxyreservatrol exerts an anti-inflammatory effect through its estrogenic-like function. In MCF-7 cells, oxyresveratrol significantly induced proliferation, which was accompanied with estrogen receptor (ER)-mediated transcriptional activation, increased estrogen-targeted gene expression (e.g., pS2, PGR, and CTSD), and increased ERα/ß proteins. The estrogen-like effect of oxyresveratrol was reversed by the ER inhibitor ICI 182780. Strong ER-binding activities of oxyresveratrol were revealed by negative docking scores. The LPS-induced inflammatory response (e.g., upregulated IκB-α phosphorylation, NF-κB nuclear translocation, and cytokine messenger RNA expression) was significantly suppressed in an ER-dependent manner by oxyresveratrol in RAW264.7 cells. These results suggest that oxyresveratrol may function as an ER agonist and modulate NF-κB signaling.

Cardioprotection against ischemia/reperfusion injury by QiShenYiQi Pill® via ameliorate of multiple mitochondrial dysfunctions.

AIM: To investigate the potential cardioprotective effects of QiShenYiQi Pill(®) (QSYQ) on myocardial ischemia/reperfusion (I/R) injury through antioxidative stress and mitochondrial protection. METHODS AND RESULTS: Sprague Dawley rats were pretreated with QSYQ or saline for 7 days and subjected to ischemia (30 minutes occlusion of the left anterior descending coronary artery) and reperfusion (120 minutes). Cardiac functions were evaluated by echocardiogram and hemodynamics. Myocardial mitochondria were obtained to evaluate changes in mitochondrial structure and function, immediately after 120 minutes reperfusion. Pretreatment with QSYQ protected against I/R-induced myocardial structural injury and improved cardiac hemodynamics, as demonstrated by normalized serum creatine kinase and suppressed oxidative stress. Moreover, the impaired myocardial mitochondrial structure and function decreased level of ATP (accompanied by reduction of ATP5D and increase in the expression of cytochrome C). Myocardial fiber rupture, interstitial edema, and infiltrated leukocytes were all significantly ameliorated by pretreatment with QSYQ. CONCLUSION: Pretreatment of QSYQ in Sprague Dawley rats improves ventricular function and energy metabolism and reduces oxidative stress via ameliorating multiple mitochondrial dysfunctions during I/R injury.

The inducible effect of LBP on maturation of dendritic cells and the related immune signaling pathways in hepatocellular carcinoma (HCC).

OBJECTIVE: To investigate the effect of LBP on differentiation and maturation of healthy human peripheral blood-derived dendritic cells cultured in different tumor microenvironment in vitro, and discuss the molecular and immunological mechanisms of LBP in treatment of tumor. METHODS: In this study, we procured the peripheral blood-derived dendritic cells precursor cell by the Density gradient centrifugation method, and used the tumor-cell supernatant to prepare conditioned medium. The GM-CSF and IL-4 induced DCs precursor cell differentiation to DCs, the TNF-α promoted the immature DCs developed to mature DCs. In this way, we detected the influence of LBP on the expressions of surface molecules of DCs cultured in different environments, and especially on the role of related-immunity and NF-κB activity. RESULTS: In LBP-treated group, the molecular phenotype of DCs, its capacity to stimulate allogeneic lymphocyte proliferation, and the levels of IL-12p70 and IFN-γ secretion were higher than the untreated group (p < 0.05), with statistical significance. Meanwhile the expression of NF-κB of the DCs in the medium treated by the LBP was higher than the untreated group (p < 0.05), also with statistical significance. Between the two different tumor microenvironment groups, the cell nucleus protein NF-κB expression is obviously different, the hepG2.2.15 group higher than the hepG2 group. CONCLUSION: LBP could increase the expression of the phenotype of DCs, the secretion of IL-12p70 and IFN-γ in MLR, and enhance the NF-κB expression, especially in the virus-related group, suggesting LBP plays the anti-tumor role stronger in the virus-related environment and this phenomenon correlates with the NF-κB signaling pathway.