Inflammatory autophagic events in cortical astrocytes: a novel target for the nutraceutical compound sulforaphane.

Impaired inflammatory responses are a common feature in many neurodegenerative diseases. For their capability of releasing and being target of pro-inflammatory molecules, astrocytes exert a key role during inflammation, affecting the development of neurodegenerative processes. A major mechanism occurring in cells for degrading self proteins and organelles is autophagy. It is known that autophagy may contribute to cell death following brain injury, is enhanced during oxidative stress and may be increased by activation of Toll-like receptors (TLR). As many pro-inflammatory molecules such as lipopolysaccaride (LPS) and interferon-gamma (IFN-gamma) are TLR ligands, autophagy might be prompted by these stimuli in astrocytes. Many nutraceutical compounds possess anti-inflammatory effects: in particular, sulforaphane (SF), an isothiocyanate of Brassica vegetables, exerts neuroprotection by inducing phase 2 enzymes and reverses oxidative stress. We examined whether inflammation triggers autophagy in astrocytes and if SF can modulate these responses.