Chlorogenic acid protects against aluminum toxicity via MAPK/Akt signaling pathway in murine RAW264.7 macrophages

Abstract

Aluminum (Al), which may bring about damage to the macrophages, has been implicated in the development of immunological diseases. It has been reported that chlorogenic acid (CGA, 5‑caffeoylquinic acid, chemical formula: C16H18O9) is a natural antioxidant and chelating agent with the capacity against Al (III)-induced biotoxicity. The present study was carried out to investigate whether CGA could reduce AlCl3-induced cellular damage in RAW264.7 cells. After treatment with AlCl3, the inhibition rate of viability and phagocytic activity of RAW264.7 cells was 54.5% and 27.6%, respectively. Administration of CGA significantly improved the integrity and phagocytic activity, and attenuated the accumulation of intracellular Al(III) level and oxidative stress in Al(III)-treated cells. Furthermore, CGA significantly inhibited Al(III)-induced increase of phospho-Jun N-terminal kinase (p-JNK), a pro-apoptotic Bcl-2 family protein (Bad), cytochrome c and decrease of extracellular regulated protein kinases (ERK1/2), protein kinase B (Akt) protein expressions. These results showed that CGA has a protective effect against Al(III)-induced cytotoxicity through mitogen-activated protein kinase (MAPK)/Akt-mediated caspase pathways in RAW264.7 cells.