An ethanolic extract of the aerial part of <i>Siegesbeckia orientalis </i>L. inhibits the production of inflammatory mediators regulated by AP-1, NF-κB and IRF3 in LPS-stimulated RAW 264.7 cells
Abstract:Herba Siegesbeckiae (HS, the dried aerial part of Siegesbeckia orientalis L.) is a commonly used traditional Chinese medicinal herb for treating inflammatory diseases. HS has been reported to exert anti-inflammatory effects by inhibiting the MAPKs and NF-κB pathways, the downstream effectors of TLR4 signalling. This study aims to further investigate the involvement of TLR4 signalling cascades in the effects of an ethanolic extract of HS (HS for short) on inflammatory mediators in murine macrophages. HS was ext… Show more
“…Once the stimulus is resolved, the process returns to the latent state. Many studies had proved that the NF-κB signaling pathway is involved in the occurrence and development of inflammation-related diseases and cancer [33,34]. To investigate the interrelation between NF-κB signaling pathway and RE, we furthermore performed western blotting assay on the esophageal tissue proteins.…”
As one of the gastroesophageal reflux disease (GERD), reflux esophagitis (RE) severely affects patients' daily lives. Costunolide (Cos), pertains to a sesquiterpene lactone, performs multiple pharmacological activities including inhibited acute liver injury, anti-inflammation and anti-oxidant. We carried out our study to investigate the anti-inflammatory effect and protective effects of Cos against esophageal tissue damage caused by gastric acid refluxing. The determination of anti-inflammatory effects of Cos were conducted using lipopolysaccharide (LPS)-induced RAW 264.7 cell inflammatory model. The ameliorative effects of Cos on RE were confirmed on RE controlled rats model. The results indicated that Cos reduced nitrite production and inhibited cellular inflammation via regulating the activation of NF-κB. In addition, gastric acid reflux increased expression levels of inflammatory proteins (COX-2, TNF-α and IL-1β) in esophageal tissues, while Cos treatment significantly downregulated the expression of these proteins by inhibiting activation of NF-κB. Furthermore, through observing histological stain, Cos significantly improved esophageal damage caused by gastric acid reflux. Therefore, we suggested that Cos has the potential to be a material of natural drug for the treatment of reflux esophagitis caused by acid reflux.
“…Once the stimulus is resolved, the process returns to the latent state. Many studies had proved that the NF-κB signaling pathway is involved in the occurrence and development of inflammation-related diseases and cancer [33,34]. To investigate the interrelation between NF-κB signaling pathway and RE, we furthermore performed western blotting assay on the esophageal tissue proteins.…”
As one of the gastroesophageal reflux disease (GERD), reflux esophagitis (RE) severely affects patients' daily lives. Costunolide (Cos), pertains to a sesquiterpene lactone, performs multiple pharmacological activities including inhibited acute liver injury, anti-inflammation and anti-oxidant. We carried out our study to investigate the anti-inflammatory effect and protective effects of Cos against esophageal tissue damage caused by gastric acid refluxing. The determination of anti-inflammatory effects of Cos were conducted using lipopolysaccharide (LPS)-induced RAW 264.7 cell inflammatory model. The ameliorative effects of Cos on RE were confirmed on RE controlled rats model. The results indicated that Cos reduced nitrite production and inhibited cellular inflammation via regulating the activation of NF-κB. In addition, gastric acid reflux increased expression levels of inflammatory proteins (COX-2, TNF-α and IL-1β) in esophageal tissues, while Cos treatment significantly downregulated the expression of these proteins by inhibiting activation of NF-κB. Furthermore, through observing histological stain, Cos significantly improved esophageal damage caused by gastric acid reflux. Therefore, we suggested that Cos has the potential to be a material of natural drug for the treatment of reflux esophagitis caused by acid reflux.
“…TLR4 can be activated by LPS, it may be the target protein of Chinese herbs, which inhibited LPS-induced in ammation in RAW264.7 cells [41]. Research about Chinese herbs found that Chinese herbs inhibited LPS-induced TLR4 and MyD88 expressions in RAW264.7 macrophages, as a result, inhibiting the production of in ammatory mediators [42,43]. Of the several transcriptional factors activated by in ammatory responses during bacterial infections, NF-κB plays a critical role in several signal transduction pathways.…”
Background: Kechuangping mixture (KCPM) based on Maxingshigan decoction has a significant clinical effect in the treatment of pediatric pneumonia, especially for asthmatic pneumonia. This study explored the effects of KCPM on lipopolysaccharide (LPS)-induced macrophage immune response and the molecular mechanism involved. Methods: CCK-8 assays was used to detect the effect of KCPM on cell viability. The RAW 264.7 macrophages were divided into four groups: blank, LPS, KCPM, LPS+KCPM. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to examine the secretion of inflammatory factors and the expression of TLR4/MyD88/NF-κB signal pathways with or without KCPM stimulation. Results: KCPM inhibited the differentiation of RAW264.7 macrophages induced by LPS. The secretion of pro-inflammatory cytokines IL-6 and TNF-α induced by LPS was decreased by pre-treatment with KCPM. While, treatment with KCPM advanced, the anti-inflammatory cytokines IL-10 and TGF-β increased significantly. Additionally, KCPM exhibited a potent inhibitory effect on the expression of iNOS and a promotive effect on the expression of Arg-1. Moreover, KCPM clearly suppressed the transcription level of TLR4, MyD88 and NF-κB signal pathways.Conclusion: KCPM promoted the macrophages polarization toward to M2 phenotype, as a result, limited the macrophage immune response. TLR4/MyD88/NF-κB signal pathways may play an important role in this process.
“…In addition, lower NO levels were detected after the GSYJ treatment than after the LPS treatment ( Figure 6(c)). [18]. GSYJ inhibits the expression of the IL-1β, IL-6, RANTES, and iNOS mRNAs in LPS-induced macrophages.…”
Section: Effects Of Gsyj On Lps-induced Changes In the Mrna And Protementioning
This study explored the potential therapeutic efficacy of GSYJ in attenuating asthma symptom severity and aimed to determine the immunomodulatory mechanism of GSYJ. A mouse model of chronic asthma induced by repeated Dermatophagoides pteronyssinus (Der p) challenge was established. In addition, 30 minutes before Der p challenge, the mice were orally administered GSYJ (1 g/kg). The mice were sacrificed to evaluate inflammatory cell infiltration, collagen deposition in the lung, total IgE in serum, and expression profiles of various cytokines in bronchoalveolar lavage fluid (BALF) and various genes in lung tissue. Furthermore, 30 minutes after the addition of GSYJ to RAW264.7 cell cultures, 100 ng/ml LPS was added to evaluate the effect of the drug on the LPS-induced expression of genes, proteins, and transcription factors. GSYJ may regulate transcription factors (cJUN/IRF3/NF-κB) to decrease the expression of IL-1β, IL-6, RANTES, and iNOS in macrophages and affect the IL-12, IFN-γ, IL-5, and IL-6 levels in the BALF of mice to relieve asthma symptoms, such as inflammatory cell infiltration, hyperresponsiveness, and increased serum total IgE levels. Therefore, GSYJ has the potential to be developed into a drug treatment for chronic asthma.
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