Epigallocatechin 3‐Gallate Inhibitory Effects on Inflammatory Mediators in BV‐2 Microglial Cells

Abstract

Chronic neuroinflammation has been associated with many neurodegenerative diseases such as Alzheimer's and Parkinson's Disease. The chronic activation of microglia can cause neuronal damage by releasing proinflammatory cytokines and reactive oxygen mediators. Epigallocatechin‐3‐Gallate (EGCG) is a bioactive polyphenol that exhibits significant anti‐inflammatory and neuroprotective properties in green tea extract. The current study aims to examine how EGCG can prevent chronic inflammation by inhibiting proinflammatory responses and oxidative stress induction. If proven to be the case, EGCG may serve as a nutraceutical for preventing neurodegenerative disorders. In this study, we evaluated the anti‐inflammatory activity of EGCG in lipopolysaccharide (LPS) stimulated BV‐2 microglia cells. BV‐2 microglial cells were first stimulated with 1µg/mL LPS for 1hr; then incubated for 24 hrs using different concentrations of EGCG. Cell viability was assessed using resazurin (Alamar™ Blue) indicator dye. In addition, inflammatory cytokines were profiled using QIAGEN mouse inflammatory cytokines multi‐analyte ELISA array, and nitric oxide (NO) release was evaluated using the Griess Reagent Assay. Our results showed that EGCG caused a concentration‐dependent decrease in cell viability of LPS stimulated BV‐2 microglia cells for EGCG concentrations higher than 150 µM. EGCG also significantly inhibited the release of the proinflammatory cytokine IL‐6 and the inflammatory mediator NO production at 150 µM, and 175µM in LPS stimulated BV‐2 microglial cells. In conclusion, EGCG has decreased IL‐6 and NO production, but further research will be performed to elucidate the anti‐inflammatory and antioxidative attributes of EGCG on inflammation‐induced neurodegenerative diseases.