Anti-inflammatory Activities of Gouania leptostachya Methanol Extract and its Constituent Resveratrol

Abstract

Gouania leptostachya DC. var. tonkinensis Pitard. Rhamnaceae is a traditional medicinal plant used in Thailand for treating various inflammatory symptoms. However, no systematic studies have been performed concerning the anti-inflammatory effects or molecular mechanisms of this plant. The immunopharmacological activities of a methanol extract from the leaves and twigs of G. leptostachya (Gl-ME) were elucidated based on the gastritis symptoms of mice treated with HCl/EtOH and the inflammatory responses, such as nitric oxide (NO) release and prostaglandin E2 (PGE2) production, from RAW264.7 cells and peritoneal macrophages. Moreover, inhibitory target molecules were also assessed. Gl-ME dose-dependently diminished the secretion of NO and PGE2 from LPS-stimulated RAW264.7 cells and peritoneal macrophages. The gastritis lesions of HCl/EtOH-treated mice were also attenuated after Gl-ME treatment. The extract (50 and 300 µg/mL) clearly reduced mRNA expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2, nuclear translocation of p65/nuclear factor (NF)-κB, phosphorylation of p65-activating upstream enzymes, such as protein kinase B (AKT), inhibitor of κBα kinase (IKK), and inhibitor of κB (IκBα), and the enzymatic activity of Src. By HPLC analysis, one of the major components in the extract was revealed as resveratrol with NO and Src inhibitory activities. Moreover, this compound suppressed NO production and HCl/EtOH-induced gastric symptoms. Therefore, these results suggest that Gl-ME might be useful as an herbal anti-inflammatory medicine through the inhibition of Src and NF-κB activation pathways. The efficacy data of G. leptostachya also implies that this plant could be further tested to see whether it can be developed as potential anti-inflammatory preparation.

Anti-Inflammatory and Antinociceptive Activities of Anthraquinone-2-Carboxylic Acid

“…Considering that ranitidine also suppresses COX-2 mRNA expression ( Figure 4(a) ), it seems likely that HCl/EtOH-induced tissue damage triggers cellular COX-2 expression. Indeed, we previously confirmed the pathophysiological role of COX-2 in HCl/EtOH-induced gastritis conditions through the ameliorative effects of treatment with the selective COX-2 inhibitor rofecoxib [ 30 ] and the flavonoid kaempferol, which also inhibits COX-2 expression (Dung et al, submitted). Further supporting these findings, AQCA effectively inhibited the expression of iNOS, TNF- α , and COX-2 in LPS-treated RAW264.7 cells ( Figure 4(b) ) and suppressed the level of COX-2 protein under the same conditions ( Figure 4(c) ), implying that AQCA primarily suppresses the expression of inflammatory mediators at the transcriptional level.…”

Src Is a Prime Target Inhibited by Celtis choseniana Methanol Extract in Its Anti‐Inflammatory Action

“…To examine the effects of Cc-ME on the activity of upstream molecules for the NF- κ B signaling pathway, we determined the phosphorylation of those upstream molecules in LPS-treated RAW264.7 cells after Cc-ME treatment using Western blot analysis and immunoprecipitation. Since I κ B α , IKK α / β , AKT, p85, and Src are known as upstream regulators of NF- κ B translocation into the nucleus, the activation of these molecules was assessed by determining their phosphorylation state using their phospho-specific antibodies as reported previously [ 40 , 41 ]. Phosphorylation of I κ B α and IKK α / β was inhibited by Cc-ME from 30 to 60 min, and phosphorylation of AKT and p85 was suppressed by Cc-ME from 5 to 60 min in the LPS-treated RAW264.7 cells (Figures 3(a) and 3(b) ).…”

Mogroside IIIE Attenuates LPS‐Induced Acute Lung Injury in Mice Partly Through Regulation of the TLR4/MAPK/NF‐κB Axis via AMPK Activation

“…Lipopolysaccharide (LPS)‐induced ALI mice are the most commonly used pharmacological research animal models, as LPS augments the production of inflammatory mediators through infiltration of inflammatory cells (Rossol et al, ; Dung et al, ; Li et al, ). Toll‐like receptor 4 (TLR4) has been identified as the pattern recognition receptor for LPS (Rhee, ).…”