Abstract
Artemisia apiacea Hance is one of the most widely used herbs for the treatment of malaria, jaundice, and dyspeptic complaint in oriental medicine. This study investigated the effects of methanol extracts of A. apiacea Hance (MEAH) on the induction of inducible nitric oxide synthase (iNOS) and proinflammatory mediators by lipopolysaccharide (LPS) in Raw264.7 macrophage cells and also evaluated the in vivo effect of MEAH on carrageenan-induced paw edema in rats. MEAH treatment in Raw264.7 cells significantly decreased LPS-inducible nitric oxide production and the expression of iNOS in a concentration-dependent manner, while MEAH (up to 100 μg/mL) had no cytotoxic activity. Results from immunoblot analyses and ELISA revealed that MEAH significantly inhibited the expression of cyclooxygenase-2, tumor necrosis factor-α, interleukin-1β, and interleukin-6 in LPS-activated cells. As a plausible molecular mechanism, increased degradation and phosphorylation of inhibitory-κBα and nuclear factor-κB accumulation in the nucleus by LPS were partly blocked by MEAH treatment. Finally, MEAH treatment decreased the carrageenan-induced formation of paw edema and infiltration of inflammatory cells in rats. These results demonstrate that MEAH has an anti-inflammatory therapeutic potential that may result from the inhibition of nuclear factor-κB activation, subsequently decreasing the expression of proinflammatory mediators.
Highlights
Inflammation is regarded as a protective response against tissue injury or destruction
This study examined the effect of methanol extracts of A. apiacea Hance (MEAH) on the expression of inflammatory mediators in LPS-stimulated Raw264.7 cells and investigated the in vivo effect of MEAH on carrageenan-induced edema formation
MTT assay indicated that treatment with MEAH up to 100 μg/mL for 24 h did not show any toxicity in Raw264.7 cells
Summary
Inflammation is regarded as a protective response against tissue injury or destruction. A number of inflammatory cells infiltrate into the damaged tissue and produce inflammatory mediators that exaggerate inflammatory responses characterized by redness, swelling, fever, and pain [1]. Nitric oxide (NO), prostanoids, tumor necrosis factor-α (TNF-α), and interleukins (ILs) produced from infiltrated cells or damaged tissue act as pleiotropic effector molecules to amplify acute inflammation and lead to the activation of adaptive immune response. It is essential that the inflammatory process must be controlled spaciotemporally to prevent unwanted tissue damage and reduce inflammation-related disorders. Nuclear factorkappa B (NF-κB) is an essential signaling molecule to increase the production of effector molecules related to acceleration of the inflammatory process [2]. Activation of NFκB in the cytoplasm allows it to translocate into the nucleus, where it binds to the promoter region of target genes that are Evidence-Based Complementary and Alternative Medicine associated with immune responses, cell survival, apoptosis, and so on [4]
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