scholarly journals Octominin Inhibits LPS-Induced Chemokine and Pro-inflammatory Cytokine Secretion from RAW 264.7 Macrophages via Blocking TLRs/NF-κB Signal Transduction

Biomolecules ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 511 ◽  
Author(s):  
K. K. Asanka Sanjeewa ◽  
D. P. Nagahawatta ◽  
Hye-Won Yang ◽  
Jae Young Oh ◽  
Thilina U. Jayawardena ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Inflammatory Cytokine ◽  
Inflammatory Responses ◽  
Signal Transduction Pathway ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Potential Candidate ◽  
Transduction Pathway ◽  
Raw 264.7 Macrophages ◽  
In Silico Docking

Inflammation is a well-organized innate immune response that plays an important role during the pathogen attacks and mechanical injuries. The Toll-like receptors (TLR)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is a major signal transduction pathway observed in RAW 264.7 macrophages during the inflammatory responses. Here, we investigated the anti-inflammatory effects of Octominin; a bio-active peptide developed from Octopus minor in RAW 264.7 macrophages in vitro. Octominin was found to inhibit lipopolysaccharides (LPS)-stimulated transcriptional activation of NF-κB in RAW 264.7 cells and dose-dependently decreased the mRNA expression levels of TLR4. Specifically, in silico docking results demonstrated that Octominin has a potential to inhibit TLR4 mediated inflammatory responses via blocking formation of TLR4/MD-2/LPS complex. We also demonstrated that Octominin could significantly inhibit LPS-induced secretion of pro-inflammatory cytokine (interleukin-β; IL-1β, IL-6, and tumor necrosis factor-α) and chemokines (CCL3, CCL4, CCL5, and CXCL10) from RAW 264.7 cells. Additionally, Octominin repressed the LPS-induced pro-inflammatory mediators including nitric oxide (NO), prostaglandin E2, inducible NO synthase, and cyclooxygenase 2 in macrophages. These results suggest that Octominin is a potential inhibitor of TLRs/NF-κB signal transduction pathway and is a potential candidate for the treatment of inflammatory diseases.

Macrophage migration inhibitory factor antagonizes hydrocortisone-induced increases in cytosolic IκBα

2000 ◽  
Vol 279 (3) ◽  
pp. R1043-R1049 ◽  
Author(s):  
Jane M. Daun ◽  
Joseph G. Cannon
Keyword(s):  
Signal Transduction ◽  
Dna Binding ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inflammatory Cytokine ◽  
Signal Transduction Pathway ◽  
Inhibitory Factor ◽  
Pituitary Cells ◽  
Macrophage Migration ◽  
Transduction Pathway

Macrophage migration inhibitory factor (MIF) is an inflammatory cytokine secreted by several cell types, including mononuclear and pituitary cells. It has also been shown to counteract cortisol-induced inhibition of inflammatory cytokine secretion. The purpose of this study was to determine whether MIF antagonized the effect of hydrocortisone on the NF-κB/IκB signal transduction pathway in lipopolysaccharide (LPS)-stimulated human peripheral blood mononuclear cells. Physiological doses of hydrocortisone (50–200 ng/ml) diminished both the LPS-stimulated decrease in cytosolic IκBα levels and the subsequent increase in nuclear NF-κB DNA binding. In the presence of both LPS and hydrocortisone, 1 ng/ml of MIF antagonized the effects of hydrocortisone, resulting in decreased cytosolic IκBα levels ( P < 0.05) and increased nuclear NF-κB DNA binding ( P < 0.05). In the absence of hydrocortisone, MIF had no effect on LPS-induced decreases in IκBα. In the absence of LPS, MIF inhibited hydrocortisone-induced increases in IκBα ( P = 0.03). Thus the mechanism by which MIF antagonizes the effect of hydrocortisone on the NF-kB/IκB signal transduction pathway is through inhibiting the ability of hydrocortisone to increase cytosolic IκBα.

scholarly journals HO-1 Induction by Selaginella tamariscina Extract Inhibits Inflammatory Response in Lipopolysaccharide-Stimulated RAW 264.7 Macrophages

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
An-Na Won ◽  
Sun Ah Kim ◽  
Jung Yun Ahn ◽  
Jae-Hyun Han ◽  
Chang-Hyun Kim ◽  
...  
Keyword(s):  
Nuclear Translocation ◽  
Inflammatory Responses ◽  
Scientific Evidence ◽  
Radical Scavenging ◽  
Raw 264.7 Cells ◽  
Ros Generation ◽  
Raw 264.7 ◽  
Raw 264.7 Macrophages ◽  
Selaginella Tamariscina ◽  
Anti Inflammatory

Selaginella Herba is the dried, aerial part of Selaginella tamariscina (P.Beauv.) Spring and has been used to treat amenorrhea, abdominal pain, headaches, and hematuria in Korea. However, scientific evidence regarding the anti-inflammatory activity and action mechanism of Selaginella tamariscina is lacking. Thus, the present study was performed to investigate the anti-inflammatory and antioxidant activities of Selaginella tamariscina ethanol extract (STE) against lipopolysaccharide (LPS)-induced inflammatory responses and identify the molecular mechanism responsible. STE was prepared by heating in 70% ethanol and its quality was confirmed by HPLC. STE dose-dependently inhibited the productions of inflammatory mediators (NO and PGE2) and proinflammatory cytokines (IL-1β and IL-6) in LPS-stimulated RAW 264.7 cells. STE markedly suppressed the phosphorylations of MAPKs, IκB-α, and NF-κB and the nuclear translocation of NF-κB induced by LPS stimulation. In addition, STE exhibited good free radical scavenging activity and prevented ROS generation by LPS. STE also upregulated the expression of Nrf2 and HO-1 and promoted the nuclear translocation of Nrf2. Taken together, STE was found to have anti-inflammatory and antioxidant effects on RAW 264.7 macrophages and the mechanism appeared to involve the MAPK, NF-κB, and Nrf2/HO-1 signaling pathways. These results suggest that STE might be useful for preventing or treating inflammatory diseases and provide scientific evidence that supports the developments of herbal prescriptions or novel natural products.

Regulation of RAW 264.7 cell-mediated immunity by polysaccharides from Agaricus blazei Murill via the MAPK signal transduction pathway

2017 ◽  
Vol 8 (4) ◽  
pp. 1475-1480 ◽  
Author(s):  
Feier Cheng ◽  
Xiaoyan Yan ◽  
Miaoqing Zhang ◽  
Mingchang Chang ◽  
Shaojun Yun ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Signal Transduction Pathway ◽  
Cell Mediated Immunity ◽  
Raw 264.7 ◽  
Transduction Pathway ◽  
Agaricus Blazei ◽  
Raw 264.7 Cell ◽  
Folk Remedy ◽  
Agaricus Blazei Murill

Agaricus blazei Murill (ABM) is a common anticancer folk remedy.

scholarly journals Dracocephalum moldavica Ethanol Extract Suppresses LPS-Induced Inflammatory Responses through Inhibition of the JNK/ERK/NF-κB Signaling Pathway and IL-6 Production in RAW 264.7 Macrophages and in Endotoxic-Treated Mice

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4501
Author(s):  
Kyeong-Min Kim ◽  
So-Yeon Kim ◽  
Tamanna Jahan Mony ◽  
Ho Jung Bae ◽  
Sang-Deok Han ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Ethanol Extract ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Septic Mouse ◽  
Raw 264.7 Macrophages ◽  
Mrna And Protein Expression ◽  
Anti Inflammatory ◽  
Underlying Mechanisms

The excessive synthesis of interleukin-6 (IL-6) is related to cytokine storm in COVID-19 patients. Moreover, blocking IL-6 has been suggested as a treatment strategy for inflammatory diseases such as sepsis. Sepsis is a severe systemic inflammatory response syndrome with high mortality. In the present study, we investigated the anti-inflammatory and anti-septic effects and the underlying mechanisms of Dracocephalum moldavica ethanol extract (DMEE) on lipopolysaccharide (LPS)-induced inflammatory stimulation in RAW 264.7 macrophages along with septic mouse models. We found that DMEE suppressed the release of inflammatory mediators NO and PGE2 and inhibited both the mRNA and protein expression levels of iNOS and COX-2, respectively. In addition, DMEE reduced the release of proinflammatory cytokines, mainly IL-6 and IL-1β, in RAW 264.7 cells by inhibiting the phosphorylation of JNK, ERK and p65. Furthermore, treatment with DMEE increased the survival rate and decreased the level of IL-6 in plasma in LPS-induced septic shock mice. Our findings suggest that DMEE elicits an anti-inflammatory effect in LPS-stimulated RAW 264.7 macrophages and an anti-septic effect on septic mouse model through the inhibition of the ERK/JNK/NF-κB signaling cascades and production of IL-6.

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