Abstract
Pyeongwisan (PW) is an herbal medication used in traditional East Asian medicine to treat anorexia, abdominal distension, borborygmus and diarrhea caused by gastric catarrh, atony and dilatation. However, its effects on inflammation-related diseases are unknown. In this study, we investigated the biological effects of PW on lipopolysaccharide (LPS)-mediated inflammation in macrophages and on local inflammation in vivo. We investigated the biological effects of PW on the production of inflammatory mediators, pro-inflammatory cytokines and related products as well as the activation of nuclear factor kappa B (NF-κB) and mitogen-activated protein kinases (MAPKs) in LPS-stimulated macrophages. Additionally, we evaluated the analgesic effect on the acetic acid-induced writhing response and the inhibitory activity on xylene-induced ear edema in mice. PW showed anti-inflammatory effects by inhibiting the production of nitric oxide (NO), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) and interleukin-1β (IL-1β). In addition, PW strongly suppressed inducible nitric oxide synthase (iNOS), a NO synthesis enzyme, induced heme oxygenase-1 (HO-1) expression and inhibited NF-κB activation and MAPK phosphorylation. Also, PW suppressed TNF-α, IL-6 and IL-1β cytokine production in LPS-stimulated peritoneal macrophage cells. Furthermore, PW showed an analgesic effect on the writhing response and an inhibitory effect on mice ear edema. We demonstrated the anti-inflammatory effects and inhibitory mechanism in macrophages as well as inhibitory activity of PW in vivo for the first time. Our results suggest the potential value of PW as an inflammatory therapeutic agent developed from a natural substance.
Highlights
Inflammation is part of a complex biological immune response that occurs in vascular tissues due to harmful stimuli such as pathogens, cellular damage and irritants [1]
nitric oxide (NO) and prostaglandin E2 (PGE2) are synthesized by inducible NO synthase and cyclooxygenase-2 (COX-2), respectively, and iNOS expression is closely related to the induction of heme oxygenase-1 (HO-1), a stress-inducible protein that catalyzes the oxidative degradation of heme
NO overproduction is associated with various inflammatory diseases [18,19], and NO inhibition can relieve inflammation; we investigated the inhibitory effects of PW on NO production induced by LPS stimulation
Summary
Inflammation is part of a complex biological immune response that occurs in vascular tissues due to harmful stimuli such as pathogens, cellular damage and irritants [1]. HO-1 expression is enhanced by free heme and by various pro-inflammatory stimulants such as NO, LPS, cytokines, heavy metals and other oxidants [6,7]. Activated NF-κB is translocated to the nucleus, where it binds to DNA promoters to induce production of inflammatory genes, including iNOS, COX-2, cytokines and chemokines [13,14]. Signaling pathway, involving extracellular signal-regulated kinase (ERK), p38 and c-Jun NH2-terminal kinase (JNK) MAPKs, plays an important role in relaying inflammatory information from the extracellular environment into the cytoplasm and nucleus [15]. We evaluated the inhibitory effect of PW on inflammatory pathway activation induced by LPS and the influence on HO-1 induction in murine macrophages. We investigated in vivo the analgesic effects and anti-inflammatory activities of orally administered PW
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