Objective:To explore the inflammatory responses of macrophages treated with Helicobacter pylori. Methods:Cytokines IL-23,IL-10,TNF-α and IL-8 in cell culture supernatant of macrophages stimulated with Helicobacter pylori were determined by ELISA kits,and the expression of intracellular proteins NOS2 and COX2 in Helicobacter pylori treated macrophages was analyzed by Western blot. Then,the apoptosis of Helicobacter pylori stimulated macrophages was detected by flow cytometry. Results:The secretion of cytokines IL-23,IL-10,TNF-α and IL-8 in the culture supernatant of Helicobacter pylori treated macrophages increased significantly (P<0. 05),and the expression of NOS2 and COX2 was enhanced evidently(P<0. 05). Meanwhile,helicobacter pylori could induce the apoptosis of macrophages obviously ( P<0. 03 ) . Conclusion: The inflammatory responses of macrophages treated with Helicobacter pylori would be promoted to inhibit or kill Helicobacter pylori,furthermore,Helicobacter pylori could induce the apotosis of macropha-ges.

Objective To study the quality standard of Folium Nelumbinis.Methods Flavonoids of Folium Nelumbinis were identified by TLC.The extraction conditions of flavonoids was studied and the content of total flavonoids was determined by ultraviolet spectrophotometry .Results Quercetin in Folium Nelumbinis was identified by TLC.The optimal extraction conditions were defined and the content of total flavonoids was about 13 %.Conclusion This method is simple and convenient, and is feasible for the quantitative determination of Folium Nelumbinis.

OBJECTIVE: To evaluate whether dexmedetomidine hydrochloride, an α2-adrenergic receptor agonist, can prevent oxidative damage to alveolar macrophages induced by H2O2. METHODS: We used methyl thiazolyl tetrazolium (MTT) colorimetry to test the effect of different concentrations and action time of H2O2 on the survival rate of alveolar macrophages, and then we chose the appropriate H2O2 concentration and action time to build NR8383 cell oxidative damage model. After pre-conditioning of 0.01, 0.10, and 1.00 μmol/L dexmedetomidine hydrochloride for 24 hours, MTT colorimetry was used to demonstrate the survival rate of NR8383 cells damaged by H2O2, and the release of lactate dehydrogenase (LDH) and TNF-α by H2O2-damaged NR8383 cells was detected by corresponding kit. RESULTS: At 50-300 μmol/L, H2O2 caused concentration-dependent oxidative damage in the alveolar macrophages, decreased the cell survival rate, and increased LDH and TNF-α release. At 0.01-1.00 μmol/L dexmedetomidine hydrochloride concentration-dependently protected NR8383 cells from oxidative damage induced by H2O2, significantly increased the cell survival rate, decreased LDH and TNF-α release, and this effect of dexmedetomidine hydrochloride was dose-dependent. Yohimbine, an α2 - adrenergic receptor antagonist, completely neutralized the protective effect of dexmedetomidine hydrochloride on NR8383 cells without affecting the oxidative damage of NR8383 cells. CONCLUSION Dexmedetomidine hydrochloride can prevent alveolar macrophages from oxidative damage induced by H2O2, which may play a protective role through α2 - adrenergic receptors.
Animals ; Cell Line ; Cell Survival ; Dexmedetomidine ; pharmacology ; Hydrogen Peroxide ; L-Lactate Dehydrogenase ; metabolism ; Macrophages, Alveolar ; drug effects ; Oxidative Stress ; Rats ; Receptors, Adrenergic, alpha-2 ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism