Anti-Inflammatory Effects of Catalpalactone Isolated from Catalpa ovata in LPS-Induced RAW264.7 Cells

Catalpa ovata (Bignoniaceae) is widely distributed throughout Korea, China, and Japan. This study investigated the anti-inflammatory effects of catalpalactone isolated from C. ovata in lipopolysaccharide (LPS)-induced RAW264.7 cells. Catalpalactone significantly inhibited nitric oxide (NO) production and inducible NO synthase (iNOS) expression in LPS-induced RAW264.7 cells. The levels of cytokines such as interleukin-6 and tumor necrosis factor-α were reduced under catalpalactone exposure in LPS-induced RAW264.7 cells. Additionally, catalpalactone suppressed signal transducer and activator of transcription 1 (STAT-1) protein expression and interferon-β (IFN-β) production. Treatment with catalpalactone prevented interferon regulatory factor 3 (IRF3) and nuclear factor-κB (NF-κB) activation. Taken together, these results suggest that the anti-inflammatory effects of catalpalactone are associated with the suppression of NO production and iNOS expression through the inhibition of IRF3, NF-κB, and IFN-β/STAT-1 activation.

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Anti-Inflammatory Effect of Simonsinol on Lipopolysaccharide Stimulated RAW264.7 Cells through Inactivation of NF-κB Signaling Pathway

Molecules ◽

10.3390/molecules25163573 ◽

2020 ◽

Vol 25 (16) ◽

pp. 3573

Author(s):

Lian-Chun Li ◽

Zheng-Hong Pan ◽

De-Sheng Ning ◽

Yu-Xia Fu

Keyword(s):

Nitric Oxide ◽

Signaling Pathway ◽

Morphological Changes ◽

Raw264.7 Cells ◽

Enzyme Linked Immunosorbent Assay ◽

Tnf Α ◽

Anti Inflammatory ◽

Factor Α ◽

Oxide Synthase ◽

Necrosis Factor

Simonsinol is a natural sesqui-neolignan firstly isolated from the bark of Illicium simonsii. In this study, the anti-inflammatory activity of simonsinol was investigated with a lipopolysaccharide (LPS)-stimulated murine macrophages RAW264.7 cells model. The results demonstrated that simonsinol could antagonize the effect of LPS on morphological changes of RAW264.7 cells, and decrease the production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) in LPS-stimulated RAW264.7 cells, as determined by Griess assay and enzyme-linked immunosorbent assay (ELISA). Furthermore, simonsinol could downregulate transcription of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 as measured by reverse transcription polymerase chain reaction (RT-PCR), and inhibit phosphorylation of the alpha inhibitor of NF-κB (IκBα) as assayed by Western blot. In conclusion, these data demonstrate that simonsinol could inhibit inflammation response in LPS-stimulated RAW264.7 cells through the inactivation of the nuclear transcription factor kappa-B (NF-κB) signaling pathway.

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Anti-Inflammatory Activity of the Phlorotannin Trifuhalol A Using LPS-Stimulated RAW264.7 Cells Through NF-κB and MAPK Main Signaling Pathways

Natural Product Communications ◽

10.1177/1934578x19849798 ◽

2019 ◽

Vol 14 (5) ◽

pp. 1934578X1984979 ◽

Cited By ~ 1

Author(s):

Kasira Phasanasophon ◽

Sang Moo Kim

Keyword(s):

Nitric Oxide ◽

Ethyl Acetate ◽

Signaling Pathways ◽

Ethyl Acetate Fraction ◽

Inflammatory Activity ◽

Raw264.7 Cells ◽

No Production ◽

Mitogen Activated Protein ◽

Anti Inflammatory ◽

Factor Α

Trifuhalol A, a phlorotannin, was extracted from Agarum cribrosum with ethyl acetate and fractionated using Sephadex LH-20 column chromatography (SF1-SF6). The ethyl acetate fraction (EAF) and SF5-containing trifuhalol A exhibited strong inhibitory activity against hyaluronidase. The anti-inflammatory activity of the phlorotannin, EAF, and SF5 was determined through the inhibition of nitric oxide (NO) production in lipopolysaccharide-stimulated RAW264.7 cells. Furthermore, the inhibition of NO production was validated by confirming the appreciable downregulation of inducible nitric oxide synthase expression. Agarum cribrosum phlorotannin also markedly suppressed the expression of cyclooxygenase-2, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α. In addition, the anti-inflammatory action was verified by examining its effects on proinflammatory signaling pathways. The activation of nuclear factor (NF)-κB and mitogen-activated protein kinases (MAPKs) was attenuated via the inhibition of NF-κB p-65, c-Jun N-terminal kinase, extracellular signal-regulated kinase 1/2, and p38 MAPK phosphorylation. Therefore, trifuhalol A is a potential source for either the prevention or the treatment of inflammation.

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Inhibitory effect of ginsenoside-Rd on carrageenan-induced inflammation in rats

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y11-127 ◽

2012 ◽

Vol 90 (2) ◽

pp. 229-236 ◽

Cited By ~ 15

Author(s):

Li Wang ◽

Yunxin Zhang ◽

Zhiping Wang ◽

Sijia Li ◽

Guangning Min ◽

...

Keyword(s):

Tumor Necrosis Factor ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Nuclear Factor Κb ◽

Prostaglandin E ◽

Nuclear Factor ◽

Ginsenoside Rd ◽

Anti Inflammatory ◽

Factor Α ◽

Necrosis Factor

A previous study reported that ginsenoside-Rd reduced the production of tumor necrosis factor-α by inhibiting nuclear factor-κB in lipopolysaccharide-activated N9 microglia in vitro. The aim of the present study was to confirm the anti-inflammatory effects and mechanisms of ginsenoside-Rd in animal experiments involving acute inflammation. The results indicated that ginsenoside-Rd at doses ranging from 12.5 to 50 mg/kg i.m. significantly inhibited the swelling of hind paws in rats for 1–6 h after the carrageenan injection. The levels of proinflammatory cytokines and proinflammatory mediators were markedly reduced by ginsenoside-Rd. Ginsenoside-Rd, when administered intramuscularly at 12.5, 25, and 50 mg/kg doses, showed signicant inhibition of carrageenan-induced production of interleukin-1β (6.91%, 45.75%, and 55.18%, respectively), tumor necrosis factor-α (37.99%, 56.39%, and 47.38%, respectively), prostaglandin E2 (22.92%, 30.12%, and 36.36%, respectively), and nitric oxide (28.27%, 44.53%, and 53.42%, respectively). In addition, ginsenoside-Rd (12.5, 25, and 50 mg/kg i.m.) effectively decreased the levels of nuclear factor-κB (6.77%, 20.28%, and 41.03%, respectively) and phosphorylation of IκBα (13.23%, 26.92%, and 41.80%, respectively) in the carrageenan-inflamed paw tissues. These results suggest that ginsenoside-Rd has significant anti-inflammatory effects in vivo, which might be due to its blocking of the nuclear factor-κB signaling pathway. Thus, it may be possible to develop ginsenoside-Rd as a useful agent for inflammatory diseases.

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Monoammonium glycyrrhizate suppresses tumor necrosis factor-α induced chemokine production in HMEC-1 cells, possibly by blocking the translocation of nuclear factor-κB into the nucleus

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2014-0022 ◽

2014 ◽

Vol 92 (10) ◽

pp. 859-865 ◽

Cited By ~ 4

Author(s):

Na Cao ◽

Tao Chen ◽

Zai-pei Guo ◽

Sha Qin ◽

Meng-meng Li

Keyword(s):

Tumor Necrosis ◽

Skin Diseases ◽

Nuclear Factor Κb ◽

Nuclear Factor ◽

Inflammatory Skin Diseases ◽

Chemokine Production ◽

Tnf Α ◽

Anti Inflammatory ◽

Factor Α ◽

Necrosis Factor

Monoammonim glycyrrhizate (MAG) derived from licorice has been shown to have anti-inflammatory properties. Chemokines are vital inflammatory mediators that are involved with endothelial damage from leukocyte infiltrates in various inflammatory skin diseases. In this study, we investigated the anti-inflammatory effects and mechanisms of MAG on tumor necrosis factor-α (TNF-α) induced chemokine production in a human dermal microvascular endothelial cell line (HMEC-1). HMEC-1 cells were treated with TNF-α, with or without MAG. The results showed that MAG suppressed TNF-α-induced chemokine (including CXCL8, CX3CL1, and CXCL16) mRNA expression in HMEC-1 cells, in a dose-dependent manner, and reduced the secretion of these chemokines in culture supernatant. Moreover, endothelial activation in the presence of MAG blocked the chemotactic activities of TNF-α-stimulated HMEC-1 cell supernatant on the migration of primary neutrophils and primary monocytes. In addition, Western blot and immunofluorescence data revealed that MAG inhibited nuclear translocation of nuclear factor-κB p65 (NF-κB p65). It is the first report to demonstrate that MAG suppresses TNF-α-induced chemokine production in HMEC-1 cells, and that the mechanism may be inhibiting the translocation of NF-κB p65 into the nucleus to prevent the starting of inflammatory signaling pathway. Our results revealed that MAG is a potential anti-inflammatory agent capable of improving inflammatory skin diseases.

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Anti-inflammatory effects of triptolide in human bronchial epithelial cells

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.2000.279.5.l958 ◽

2000 ◽

Vol 279 (5) ◽

pp. L958-L966 ◽

Cited By ~ 59

Author(s):

Guohua Zhao ◽

Laszlo T. Vaszar ◽

Daoming Qiu ◽

Lingfang Shi ◽

Peter N. Kao

Keyword(s):

Cell Cycle ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Nuclear Factor Κb ◽

Nuclear Factor ◽

Human Bronchial Epithelial Cells ◽

Bronchial Epithelial ◽

Anti Inflammatory ◽

Factor Α ◽

Necrosis Factor

Triptolide (PG490, 97% pure) is a diterpenoid triepoxide with potent anti-inflammatory and immunosuppressive effects in transformed human bronchial epithelial cells and T cells (Qiu D, Zhao G, Aoki Y, Shi L, Uyei A, Nazarian S, Ng JC-H, and Kao PN. J Biol Chem 274: 13443–13450, 1999). Triptolide, with an IC50of ∼20–50 ng/ml, inhibits normal and transformed human bronchial epithelial cell expression of interleukin (IL)-6 and IL-8 stimulated by phorbol 12-myristate 13-acetate (PMA), tumor necrosis factor-α, or IL-1β. Nuclear runoff and luciferase reporter gene assays demonstrate that triptolide inhibits IL-8 transcription. Triptolide also inhibits the transcriptional activation, but not the DNA binding, of nuclear factor-κB. A cDNA array and clustering algorithm analysis reveals that triptolide inhibits expression of the PMA-induced genes tumor necrosis factor-α, IL-8, macrophage inflammatory protein-2α, intercellular adhesion molecule-1, integrin β6, vascular endothelial growth factor, granulocyte-macrophage colony-stimulating factor, GATA-3, fra-1, and NF45. Triptolide also inhibits constitutively expressed cell cycle regulators and survival genes cyclins D1, B1, and A1, cdc-25, bcl-x, and c-jun. Thus anti-inflammatory, antiproliferative, and proapoptotic properties of triptolide are associated with inhibition of nuclear factor-κB signaling and inhibition of genes known to regulate cell cycle progression and survival.

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Anti-Inflammatory Activity of the Methanol Extract of Moutan Cortex in LPS-Activated Raw264.7 Cells

Evidence-based Complementary and Alternative Medicine ◽

10.1093/ecam/nel093 ◽

2007 ◽

Vol 4 (3) ◽

pp. 327-333 ◽

Cited By ~ 64

Author(s):

Seung-Chul Chun ◽

Seon Young Jee ◽

Sang Gon Lee ◽

Sook Jahr Park ◽

Jong Rok Lee ◽

...

Keyword(s):

Blood Stasis ◽

Experimental Period ◽

Nuclear Factor Κb ◽

Raw264.7 Cells ◽

Prostaglandin E ◽

Methanolic Extracts ◽

Moutan Cortex ◽

Cox 2 ◽

Anti Inflammatory ◽

Factor Α

Moutan Cortex (MCE) has been used in traditional medicine to remove heat from the blood, promote blood circulation and alleviate blood stasis. This study was conducted to evaluate the effects of MCE on regulatory mechanisms of cytokines and nitric oxide (NO) involved in immunological activity of Raw264.7 cells. Cells were pretreated with methanolic extracts of MCE, and further cultured for an appropriate time after lipopolyssacharide (LPS) addition. During the entire experimental period, 0.1 and 0.3 mg ml−1of MCE had no cytotoxicity. In these concentrations, MCE inhibited the production of NO and prostaglandin E2(PGE2), the expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2) and phosphorylated inhibitor of κBα (p-IκBα), and the activation of nuclear factor κB (NF-κB). MCE also reduced the concentration of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) in the Raw264.7 cells that were activated by LPS. These results demonstrate that MCE has anti-inflammatory effects through the inhibition of iNOS and COX-2 expression by suppressing the phosphorylation of I-κBα and the activation of NF-κB.

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Synergy between Interferon-γ and Tumor Necrosis Factor-α in Transcriptional Activation Is Mediated by Cooperation between Signal Transducer and Activator of Transcription 1 and Nuclear Factor κB

Journal of Biological Chemistry ◽

10.1074/jbc.272.23.14899 ◽

1997 ◽

Vol 272 (23) ◽

pp. 14899-14907 ◽

Cited By ~ 287

Author(s):

Yoshihiro Ohmori ◽

Robert D. Schreiber ◽

Thomas A. Hamilton

Keyword(s):

Tumor Necrosis Factor ◽

Transcriptional Activation ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Nuclear Factor Κb ◽

Interferon Γ ◽

Nuclear Factor ◽

Signal Transducer ◽

Factor Α ◽

Necrosis Factor

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Anti-Inflammatory Effect of 4,5-Dicaffeoylquinic Acid on RAW264.7 Cells and a Rat Model of Inflammation

Nutrients ◽

10.3390/nu13103537 ◽

2021 ◽

Vol 13 (10) ◽

pp. 3537

Author(s):

Goeun Jang ◽

Seulah Lee ◽

Joonho Hong ◽

Boram Park ◽

Dokyung Kim ◽

...

Keyword(s):

Nitric Oxide ◽

Nuclear Factor Κb ◽

Raw264.7 Cells ◽

Dicaffeoylquinic Acid ◽

Inflammatory Drugs ◽

Anti Inflammatory ◽

Factor Α ◽

Oxide Synthase

Anti-inflammatory agents that are safer and more effective than the currently used non-steroidal anti-inflammatory drugs are urgently needed. The dicaffeoylquinic acid (diCQA) isomer 4,5-diCQA exhibits antioxidant activity and various other health-promoting benefits; however, its anti-inflammatory properties require further investigation. This study was conducted to evaluate the anti-inflammatory properties of 4,5-diCQA in vitro and in vivo using RAW264.7 cells and a carrageenan-induced inflammation model, respectively. In RAW264.7 cells, 4,5-diCQA pretreatment significantly inhibited lipopolysaccharide-induced expression of nitric oxide, prostaglandin E2, nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-α, interleukin-1β, and interleukin-6, without inducing cytotoxicity. The inhibitory effects of 4,5-diCQA were mediated by the suppression of nuclear factor-κB nuclear translocation and mitogen-activated protein kinase (MAPK) phosphorylation. Oral administration of 4,5-diCQA at doses of 5, 10, and 20 mg/kg of the body weight suppressed carrageenan-induced edema and the expression of nitric oxide synthase, cyclooxygenase-2, and tumor necrosis factor-α in a dose-dependent manner. Collectively, our results suggest that 4,5-diCQA exerts anti-inflammatory effects by suppressing activation of the nuclear factor-κB and MAPK pathways in vitro and reducing carrageenan-induced edema in vivo. Therefore, 4,5-diCQA shows potential as a natural alternative to non-steroidal anti-inflammatory drugs.

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