利福平-abs816842

一、产品概述

二、产品信息

Rifampin inhibits IκBα degradation and mitogen-activated protein kinase (MAPK) phosphorylation. Rifampin is found to bind to human MD-2 in a Rifampin and MD-2 concentration-dependent manner. Rifampin inhibits NF-κB activation induced by LPS (20 ng/ml) in a dose-dependent manner, with an IC50 of 44.1 μM in Blue hTLR4 293 cells (A) and immunocompetent microgial BV-2 cell. Rifampin (50 μM) suppresses NF-κB activation at varying LPS doses, and the maximum NF-κB level induced by LPS in the presence of Rifampin (50 μM) is much lower than that in the absence of Rifampin. Rifampin inhibits NO production induced by LPS (200 ng/ml) in a dose-dependent manner in BV-2 cells, with an IC50 of 21.2 μM. Rifampin suppresses LPS induced TNF-α and IL-1β production in both microglia BV-2 and RAW 264.7 macrophage cells. Rifampin-inhibiting innate immune signaling is independent of the pregnane X receptor NR1I2. Rifampin combined with polyester vascular prostheses (PVP) functionalised with cyclodextrin (PVP-CD) results in significant bacterial adhesion reduction and growth inhibition against Gram-positive bacteria. Rifampin (50 μg/mL) significantly reduces the CFU counts of stationary-phase cultures and reduces the CFU counts of the log-phase culture to zero. Rifampin is particularly suitable since it is bactericidal and starts killing M. tuberculosis within an hour of exposure.

Rifampicin (200, 400 mg/kg) can induce fatty liver at high concentration. Rifampicin (30 mg/kg, i.p.) treatment of S464P biofilms in vivo results in a slight decline, but earlier rebinds in bioluminescence from these catheters compared with the parental signal, whereas rifampicin has no affect on bioluminescence in mice infected with mutant H481Y.

三、背景

四、制备和贮存

五、产品特点

六、注意事项