The Hydroalcoholic Extract Obtained from Mentha piperita L. Leaves Attenuates Oxidative Stress and Improves Survival in Lipopolysaccharide-Treated Macrophages

Figure 4

Mechanisms of action of LHAE on macrophage-mediated responses. (a) As part of the host’s immune response during bacterial infections, macrophages are activated by bacteria-derived products, such as lipopolysaccharide (LPS); and as a result of this activation, reactive species are formed. Superoxide (O₂⁻) anion produced by NADPH oxidase is converted to hydrogen peroxide (H₂O₂) by superoxide dismutase (SOD). H₂O₂ can, in turn, be further reduced to H₂O by glutathione peroxidase (GPx) or even render hydroxyl radical (HO^.), a much more potent oxidant that can lead to diminished cell survival via peroxidation (and further breakdown) of lipids, as well as oxidation of protein and DNA bases. In parallel, nitric oxide (NO^.) continuously produced by inducible NO synthase (iNOS) can react with O₂⁻ and form peroxynitrous acid (ONOOH) which, after homolytic breakdown, can also render HO^.in addition to the highly reactive nitro (NO₂^.) radical (a potent modifier of proteins and lipids), thus potentiating cell death. (b) The incubation of LPS-stimulated macrophages with LHAE does not affect NO formation but rather increases SOD and GPx activities (thus lowering O₂⁻ and H₂O₂ availability). As a consequence, OH and/or NO₂^.formation is avoided, thus improving macrophage survival.

(a)

(b)