Key result
CAPE improves cell viability and inhibits nitric oxide and peroxynitrite production in sepsis mouse models.
Why the study?
Excessive free radical production and peroxynitrite-induced cell death contribute to tissue injury during sepsis, and the therapeutic potential of CAPE to scavenge peroxynitrite was examined.
Does Caffeic acid phenethyl ester (CAPE) reduce peroxynitrite production and improve cell viability in in vitro and in vivo models of sepsis?
Population
RAW 264.7 murine macrophages stimulated with lipopolysaccharide/interferon-γ and two mouse sepsis models
Comparison
Caffeic acid phenethyl ester (CAPE) treatment vs no CAPE
Design
Preclinical in vitro and in vivo experimental study
Authors
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CAPE attenuates sepsis injury in mice but should not change practice; leaves open human translation and prospective trials.
Does Caffeic acid phenethyl ester (CAPE) reduce peroxynitrite production and improve cell viability in in vitro and in vivo models of sepsis?
CAPE attenuates inflammatory responses and cell damage by suppressing cytotoxic molecules such as nitric oxide and peroxynitrite in preclinical models of sepsis.
Kassim et al. (2014) studied Sepsis. Caffeic Acid Phenethyl Ester (CAPE) was evaluated on Peroxynitrite production and cell viability. Caffeic acid phenethyl ester (CAPE) significantly improved cell viability and inhibited nitric oxide and peroxynitrite production in vitro and in mouse models of sepsis.
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