n propyl gallate/inflamație

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Anti-inflammatory activity of n-propyl gallate through down-regulation of NF-κB and JNK pathways.

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The present study aimed to assess anti-inflammatory activity and underlying mechanism of n-propyl gallate, the n-propyl ester of gallic acid. n-Propyl gallate was shown to contain anti-inflammatory activity using two experimental animal models, acetic acid-induced permeability model in mice, and air

n-Propyl gallate suppresses lipopolysaccharide-induced inducible nitric oxide synthase activation through protein kinase Cδ-mediated up-regulation of heme oxygenase-1 in RAW264.7 macrophages.

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n-Propyl gallate is a synthetic phenolic antioxidant with potential anti-inflammatory effects. However, the underlying mechanism remains largely unknown. In the present study, we showed that n-propyl gallate increases the expression and activity of the heme oxygenase-1 (HO-1), a stress-inducible

Gallic acid-based alkyl esters synthesis in a water-free system by celite-bound lipase of Bacillus licheniformis SCD11501.

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Gallic acid (3, 4, 5- trihydroxybenzoic acid) is an important antioxidant, anti-inflammatory, and radical scavenging agent. In the present study, a purified thermo-tolerant extra-cellular lipase of Bacillus licheniformis SCD11501 was successfully immobilized by adsorption on Celite 545 gel matrix

Effect of butylated hydroxytoluene and other antioxidants on mouse lung metabolism.

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Toxic doses of butylated hydroxytoluene (BHT), a phenolic antioxidant commonly used as a food additive, are known to produce lung damage. In this study, 3 days after a single ip injection of 62.5, 215, or 500 mg/kg BHT in mice there was a dose-dependent increase in lung weight. This concentration

The amplified chemiluminescence test to characterize antirheumatic drugs as oxygen radical scavengers.

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High levels of reactive oxygen species (ROS) are generated by phagocytes involved in host defence and inflammation. Thus, it appears highly desirable to learn more about the potential of antirheumatic drugs to scavenge ROS or to inhibit their enzymatic generation. Amplified chemiluminescence (CL)

RIG-I contributes to the innate immune response after cerebral ischemia.

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BACKGROUND Focal cerebral ischemia induces an inflammatory response that when exacerbated contributes to deleterious outcomes. The molecular basis regarding the regulation of the innate immune response after focal cerebral ischemia remains poorly understood. METHODS In this study we examined the

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