Abstract

Abstract Raspberry extract is known for its anti-inflammatory effects, but its effectiveness against pathogenic Escherichia coli-induced inflammasome activation in epithelial cells is largely unknown. This study showed that raspberry extract treatment prevented oxidative stress in Caco-2 cells infected by E. coli O157:H7 and had prophylactic effects against E. coli O157:H7-induced NLRP3 inflammasome activation. In addition, raspberry extract mitigated reduction of nuclear translocation of nuclear factor erythroid 2-related factor 2 (NRF2), a key transcription factor regulating antioxidant protein expression and nitric oxide production in Caco-2 cells upon E. coli O157:H7 infection. However, raspberry extract failed to restore NRF2 nuclear content or nitric oxide production in Caco-2 cells in the presence of aminoguanidine hydrochloride, an iNOS inhibitor. Collectively, raspberry extract treatment suppressed NLRP3 mediated inflammatory response and oxidative stress in Caco-2 cells induced by E. coli O157:H7 infection. These protective effects were partially mediated by enhanced NRF2 signaling pathway and nitric oxide production.

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