Abstract
Hedyotis diffusa is a folk herb that is used for treating inflammation-related diseases in Asia. Previous studies have found that iridoids in H. diffusa play an important role in its anti-inflammatory activity. This study aimed to investigate the anti-inflammatory effect and potential mechanism of five iridoids (asperuloside (ASP), asperulosidic acid (ASPA), desacetyl asperulosidic acid (DAA), scandoside methyl ester (SME), and E-6-O-p-coumaroyl scandoside methyl ester (CSME)) that are presented in H. diffusa using lipopolysaccharide (LPS)—induced RAW 264.7 cells. ASP and ASPA significantly decreased the production of nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in parallel with the inhibition of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), TNF-α, and IL-6 mRNA expression in LPS-induced RAW 264.7 cells. ASP treatment suppressed the phosphorylation of the inhibitors of nuclear factor-kappaB alpha (IκB-α), p38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK). The inhibitory effect of ASPA was similar to that of ASP, except for p38 phosphorylation. In summary, the anti-inflammatory effects of ASP and ASPA are related to the inhibition of inflammatory cytokines and mediators via suppression of the NF-κB and mitogen-activated protein kinase (MAPK) signaling pathways, which provides scientific evidence for the potential application of H. diffusa.
Highlights
Inflammation is a natural defense response against bacteria, viral, and fungal infections [1].During the development of inflammation, macrophages can be recruited to inflammatory sites and play an essential role by stimulating intracellular cascades of cytokines and chemokines via various signals [2,3]
Toscavenge date, numerous natural products have Among been identified as potential anti-inflammatory that can inflammatory mediators them, iridoids play an important role in agents that can scavenge inflammatory mediators
asperulosidic acid (ASPA) and ASP significantly suppressed tumor necrosis factor-α (TNF-α) and IL-6 mRNA expression. These results suggested that ASPA and ASP exerted an anti-inflammatory effect through the inhibition of inducible nitric oxide synthase (iNOS), COX-2, TNF-α, and IL-6 mRNA expression
Summary
During the development of inflammation, macrophages can be recruited to inflammatory sites and play an essential role by stimulating intracellular cascades of cytokines and chemokines via various signals [2,3]. Lipopolysaccharide (LPS) is one of the most common inflammatory triggers derived from Gram-negative bacteria. It can cause multiple inflammatory reactions by activating macrophages [4] and results in the increase of inflammatory mediators, such as nitric oxide (NO). There is good evidence that nuclear factor-kappaB (NF-κB) and mitogen-activated protein kinases (MAPKs) are two crucial signaling pathways in the inflammatory process induced by LPS [5,8,9]. The gene expression of pro-inflammatory cytokine is
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