Lai X.,Jinan University |
Ye Y.,Jinan University |
Sun C.,Shandong New Times Pharmaceutical CO. |
Huang X.,Jinan University |
And 4 more authors.
International Immunopharmacology | Year: 2013
Icaritin, an intestinal metabolite of prenylflavonoids from Herba Epimedii, has been known to regulate many cellular processes. The purpose of this study was to investigate the protective effects of icaritin on inflammation in lipopolysaccharide (LPS) stimulated mouse peritoneal macrophages in vitro and zymosan induced peritonitis model in vivo. The release of Nitric oxide (NO) was measured by a Griess reagent system. The phagocytosis, the expression of CD69, the production of inflammatory cytokines and the leukocytes numbers were determined by flow cytometry. The Ca2 + influx was recorded by confocal microscopy. The phosphorylation of p38, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK) was determined by Western blot. The results showed that icaritin significantly inhibited the NO, IL-6, IL-10 TNF-α, and MCP-1 production both in vitro and in vivo. Icaritin efficiently diminished the uptake of nonopsonized pHrodo™-labeled Escherichia coli bacteria on the LPS-stimulated macrophages. In addition, icaritin significantly inhibited the expression of CD69 on CD11b+ macrophages. Icaritin pretreatment significantly inhibited the elevation of intracellular Ca2 + induced by LPS. Furthermore, icaritin markedly decreased phospho-p38 and JNK protein expression in LPS-stimulated mouse peritoneal macrophages. In vivo study, it was also observed that icaritin prolonged survival of peritonitis mice, and inhibited massive leukocyte influx into the peritoneal cavity. These results suggest that icaritin possesses significant anti-inflammatory effects that may be mediated through the regulation of inflammatory cytokines and phosphorylation of p38 and JNK. © 2013 Elsevier B.V. All rights reserved. Source
Shi Y.,Shandong New Times Pharmaceutical CO. |
Su J.,Shandong New Times Pharmaceutical CO. |
Chen J.,Shandong New Times Pharmaceutical CO. |
Xu S.,Shandong New Times Pharmaceutical CO. |
And 4 more authors.
Chinese Journal of Environmental Engineering | Year: 2014
Advanced treatment of pharmaceutical wastewater biochemical effluent was studied by using ferric-carbon micro-electrolysis-Fenton combined process. Effects of initial pH, aeration rate and reaction time of micro-electrolysis on effluent Fe2+ and Fe3+ concentration variation, COD degradation rate and subsequent Fenton oxidation process were discussed. Theory of adding sulfuric acid intermittently was proposed in order to optimize the combined process of micro-electrolysis-Fenton oxidation. Degradation rate of COD and Fe2+ concentration were improved by adding sulfuric acid intermittently to micro-electrolysis system, that got better COD removal rate of Fenton oxidation without adding FeSO4·7H2O. The results showed that, when initial pH=2.5, aeration rate was 0.6 m3/h, adding sulfuric acid was 30 min/time, micro-electrolysis reaction was 2 h, Fenton oxidation was 2 h by adding 1 mL/L H2O2, the effluent COD removal rate achieved 81.33%. Adding sulfuric acid 30 min/time to micro-electrolysis system could increase effluent Fe2+ concentration from 50 mg/L to 151 mg/L, COD degradation rate from 10.6 mg COD/(L·h) to 22.2 mg COD/(L·h). Source