Abstract
Inflammation is a fundamental process for defending against foreign antigens that involves various transcriptional regulatory processes as well as molecular signaling pathways. Despite its protective roles in the human body, the activation of inflammation may also convey various diseases including autoimmune disease and cancer. Sorbaria kirilowii is a plant originating from Asia, with no anti-inflammatory activity reported. In this paper, we discovered an anti-inflammatory effect of S. kirilowii ethanol extract (Sk-EE) both in vivo and in vitro. In vitro effects of Sk-EE were determined with lipopolysaccharide (LPS)-stimulated RAW264.7 cells, while ex vivo analysis was performed using peritoneal macrophages of thioglycollate (TG)-induced mice. Sk-EE significantly reduced the nitric oxide (NO) production of induced macrophages and inhibited the expression of inflammation-related cytokines and the activation of transcription factors. Moreover, treatment with Sk-EE also decreased the activation of proteins involved in nuclear factor (NF)-κB signaling cascade; among them, Src was a prime target of Sk-EE. For in vivo assessment of the anti-inflammatory effect of Sk-EE, HCl/EtOH was given by the oral route to mice for gastritis induction. Sk-EE injection dose-dependently reduced the inflammatory lesion area of the stomach in gastritis-induced mice. Taking these results together, Sk-EE exerts its anti-inflammatory activity by regulating intracellular NF-κB signaling pathways and also shows an authentic effect on reducing gastric inflammation.
Highlights
Inflammation is an innate immune process of eliminating foreign pathogens and repairing damaged body tissues or cells
LPS was used as the stimulating ligand for TLR4 in murine macrophage cell line RAW264.7 cells and mouse-derived peritoneal macrophages
Under LPS-induced conditions, NO production levels of RAW264.7 cells and peritoneal macrophages were dose-dependently reduced by indicated concentrations of S. kirilowii ethanol extract (Sk-EE) treatment (Figure 1a). l-NAME, a nitric oxide synthesis inhibitor [44], was used as a positive control. l-NAME (0.5, 1, and 2 mM) treatment significantly reduced NO production in both RAW264.7 cells and peritoneal macrophages in a dose-dependent manner (Figure 1b), as previously reported
Summary
Inflammation is an innate immune process of eliminating foreign pathogens and repairing damaged body tissues or cells. Microbial species possess conserved structures on their cell membrane or cell wall, called pathogen-associated molecular patterns (PAMPs), which are recognized by inflammation-related receptors. Pattern recognition receptors (PRRs), are one kind of these receptors, which are responsible for the detection of PAMPs and the initiation of intracellular signaling process for the onset of inflammation [4,5,6]. Toll-like receptors (TLRs) are transmembrane proteins that include one demonstrative family of PRRs; in humans, 10 different TLRs have been identified. Lipopolysaccharide (LPS), a type of PAMPs from Gram-negative bacteria, is a potential ligand for TLR4. The recognition of LPS by TLR4 initiates sequential intracellular signaling processes critical for inflammation [4,8,9,10,11]
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