Berberine inhibits inflammatory activation of rat brain microglia

Chronic activation of microglial cells endangers neuronal survival through the release of various proinflammatory and neurotoxic factors. Berberine, the effective ingredient of Coptidis Rhizoma and Cortex Phellodendri, has a wide range of pharmacological functions, including anti-inflammatory, anti-atherosclerotic and anti-cancer effects. The neuroprotective potential of berberine has previously been demonstrated. The present study aimed to examine whether berberine could repress microglial activation and can be considered a potential therapeutic candidate to target neurodegenerative diseases. Primary microglial cells and BV2 microglial cells were cultured and stimulated with bacterial lipopolysaccharide (LPS). Berberine chloride was treated prior to LPS or simultaneously with LPS stimulation. Results revealed that berberine was effective at inhibiting nitric oxide release from primary microglial cells when cells were exposed to the compound prior to LPS or simultaneously with LPS. It also reduced the LPS-stimulated production of tumor necrosis factor-α, interleukin-1β, prostaglandin E₂, and intracellular reactive oxygen species and nuclear factor-kappa activation. Additionally, berberine reduced nitric oxide release from microglia stimulated with interferon-γ and amyloid β. These results suggest that berberine provides neuroprotection by reducing the production of various neurotoxic molecules from activated microglia.