Abstract
Tricholoma matsutake is an edible fungus that contains various bioactive substances, some of them with immunostimulatory properties. Presently, there is limited knowledge about the functional components of T. matsutake. Our aim was to evaluate the protective effects and molecular mechanisms of two T. matsutake-derived peptides, SDLKHFPF and SDIKHFPF, on lipopolysaccharide (LPS)-induced mitochondrial dysfunction and inflammation in RAW264.7 macrophages. Tricholoma matsutake peptides significantly ameliorated the production of inflammatory cytokines and inhibited the expression of COX-2, iNOS, IKKβ, p-IκB-α, and p-NF-κB. Immunofluorescence assays confirmed the inhibitory effect of T. matsutake peptides on NF-κB/p65 nuclear translocation. Furthermore, the treatment with T. matsutake peptides prevented the accumulation of reactive oxygen species, increased the Bcl-2/Bax ratio, reversed the loss of mitochondrial membrane potential, and rescued abnormalities in cellular energy metabolism. These findings indicate that T. matsutake peptides can effectively inhibit the activation of NF-κB/COX-2 and may confer an overall protective effect against LPS-induced cell damage.
Highlights
Inflammation is a complex biological process triggered in response to various external stimuli
We determined the expression of inducible nitric oxide synthase (iNOS) and COX-2 proteins in LPS-induced RAW264.7 macrophages
We observed the LPS-induced overexpression of iNOS and COX-2 proteins, consistent with the production of Nitric oxide (NO), whereas this effect was significantly attenuated in cells pretreated with T. matsutake peptides (Figure 1B)
Summary
Inflammation is a complex biological process triggered in response to various external stimuli. Excessive and persistent inflammation can lead to diseases [1]. Stimulation of macrophages by endotoxin lipopolysaccharides (LPS) elicits multiple inflammatory responses, activates intracellular signaling cascades, and promotes the release of large amounts of pro-inflammatory cytokines [3]. Several key disease pathogenesis factors, including inflammation, mitochondrial dysfunction, protein folding dysfunction, oxidative stress, and programmed cell death, have been proposed as contributing to disease progression [4]. A previous study showed that an imbalance in intracellular antioxidant enzymes is conducive to the accumulation of reactive oxygen species (ROS) in LPS-induced inflammation [5]. Mitochondria are the main source of intracellular ROS, making them susceptible to oxidative damage [6]. Excessive ROS can cause depolarization of the mitochondrial membrane and induce oxidative stress [7]. Mitochondrial damage can lead to cell death and, in multicellular organisms, organ damage [8]
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