Inhibition of Nitric Oxide and Tumor Necrosis Factor-Alpha by Moutan Cortex in Activated Mouse Peritoneal Macrophages

Abstract

Moutan cortex, (MC) is one of the most widely used Oriental herbal medicines for treating inflammatory diseases. In this study, the effect of MC on lipopolysaccharide (LPS) and recombinant interferon‐gamma (rIFN‐γ)‐induced production of nitric oxide (NO) and tumor necrosis factor (TNF)‐alpha were examined using mouse peritoneal macrophages. MC inhibited the LPS/rIFN‐γ‐induced expression of inducible nitric oxide synthase (iNOS) and TNF‐alpha release. To clarify the mechanism involved, the effect of MC on the activation of nuclear factor (NF)‐kappaB was examined. The LPS/rIFN‐γ‐induced activation of NF‐kappaB was almost completely blocked by MC at 0.5 mg/ml. These findings demonstrate that the inhibition of the LPS/rIFN‐γ‐induced production of NO and TNF‐alpha by MC is due to the inhibition of NF‐kappaB activation.

Amelioration of Age Associated Neuroinflammation on Long Term Bacosides Treatment

“…Recently, in one of the study the triterpenoid and bacoside enriched fraction of Bacopa monnieri were found to inhibit the lipopolysaccharide (LPS) induced TNF-a production in a concentration dependant manner in mononuclear cells. The study also postulated that triterpenoid and bacoside fractions exerted this inhibitory effect in part due to their activity over NF-jB pathway, which in turn coordinates the expression of pro-inflammatory cytokines genes [14,21]. The present research findings were in accordance with the previous study and support the proposed hypothesis.…”

Inhibition of pro-inflammatory mediators: role of Bacopa monniera (L.) Wettst

“…The precise mechanism through which the triterpenoid and bacoside fractions inhibit pro-inflammatory mediator release is not clear. However, we postulate that the triterpenoid and bacoside fractions may mediate inhibitory effects on IL-6 and TNF-a protein production, at least in part, through the suppression of NF-jB activity, as NF-jB in association with other transcription factors coordinates the expression of genes that encode pro-inflammatory mediators (Chung et al 2007).…”

“…Overproduction of NO x and pro-inflammatory cytokines has been correlated with oxidative stress and pathophysiology of various diseases including arthritis, sepsis and chronic inflammation (Chung et al 2007). Inhibition of such pro-inflammatory mediators is therefore a potential therapeutic approach for the treatment of inflammatory diseases.…”

Inhibition effects of Moutan Cortex Radicis on secretion of eotaxin in A549 human epithelial cells and eosinophil migration

“…Following previous our publication (Chung et al, 2007), MCR suppresses the LPS/rIFN-␥-induced activation of NF-B in mouse peritoneal macrophages and other study revealed that eotaxin was mediated through the NF-B and p38/MAPK signaling pathway (Wong et al, 2002). To elucidate the intracellular signaling mechanism regulating the induction of eotaxin by MCR in TNF-␣, IL-4 and IL-1␤ stimulated A549 cells we performed western blot analysis.…”