EGCG Inhibits Inflammation Independently of AMPK (87.10)

Abstract

Abstract Epigallocatechin-3-gallate (EGCG), a bioactive component of green tea, has been reported to exert anti-inflammatory effects in immune cells. EGCG has been shown to activate the metabolic regulator, AMP-activated protein kinase (AMPK). Mesangial cells from MRL/lpr lupus-like mice are hyper-responsive to immune stimulation and overproduce nitric oxide (NO) and other inflammatory mediators when stimulated. In our current studies, we sought to determine if EGCG would inhibit inflammation in AMPK deficient mesangial cells. Cultured mesangial cells from MRL/lpr mice were treated with siRNA for mouse Prkaa2-Design A, specific for AMP-activated protein kinase-alpha (AMPK-α) or siRNA negative control for mouse. After 48 hours, the cells were serum-starved for 2 hours, treated with 50 μM epigallocatechin-gallate (EGCG) for one hour, and stimulated with lipopolysaccharide (LPS)/interferon (IFN)-γ for 30 minutes. The addition of siRNA inhibited AMPK expression in mesangial cells. LPS/IFN-γ induced inflammatory mediator production (iNOS expression, supernatant NO, and interleukin-6) as expected. Interestingly, EGCG blocked inflammatory mediator production in the AMPK deficient cells suggesting EGCG inhibits inflammatory pathways independently of AMPK to decrease inflammatory mediatory production. Taken together, these studies show that EGCG attenuated inflammation in MRL/lpr mouse mesangial cells independent of AMPK.