Inhibition of chikusetsusaponin IVa on inflammatory responses in RAW264.7 cell line via MAPK pathway

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Guangren Xu ◽  
Hongyu Lei ◽  
Qiaoling Yuan ◽  
Huiyu Chen ◽  
Jianming Su
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Responses ◽  
Mapk Pathway ◽  
Biological Activities ◽  
Interleukin 10 ◽  
Raw264.7 Cell ◽  
Anti Inflammatory ◽  
Underlying Mechanisms ◽  
Factor Α ◽  
Oxide Synthase

AbstractChikusetsusaponin IVa (CHS-IVa), a saponin from herb Panacis japonicas, possesses extensive biological activities. However, the roles and underlying mechanisms of CHS-IVa on inflammation have not been fully clarified in the setting of murine macrophages. In this study, we found that CHS-IVa effectively reduced the expression of inflammatory mediators, including interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), interleukin-1β (IL-1β), cyclooxygenase (COX-2), inducible nitric oxide synthase (iNOS) in lipopolysaccharide (LPS)-stimulated murine macrophage-like RAW264.7 cells. Meanwhile, CHS-IVa could also evidently bate the contents of nitric oxide (NO) and prostaglandin E2 (PGE2) in cell culture supernatants. Furthermore, the anti-inflammatory activity of CHS-IVa may be via diminishing the phosphorylation of extracellular regulated protein kinases (ERK), p38, and c-Jun N-terminal kinase (JNK). Collectively, these findings will help to understand of the anti-inflammatory effects and mechanisms of P. japonicas deeply, and suggest a validated therapeutic use as an anti-inflammatory medication.

scholarly journals Phytosterols Suppress Phagocytosis and Inhibit Inflammatory Mediators via ERK Pathway on LPS-Triggered Inflammatory Responses in RAW264.7 Macrophages and the Correlation with Their Structure

Foods ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 582 ◽  
Author(s):  
Yuan ◽  
Zhang ◽  
Shen ◽  
Jia ◽  
Xie
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Responses ◽  
Ester Group ◽  
No Production ◽  
Raw264.7 Macrophages ◽  
Extracellular Signal ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase

Phytosterols, found in many commonly consumed foods, exhibit a broad range of physiological activities including anti-inflammatory effects. In this study, the anti-inflammatory effects of ergosterol, β-sitosterol, stigmasterol, campesterol, and ergosterol acetate were investigated in lipopolysaccharide (LPS)-induced RAW264.7 macrophages. Results showed that all phytosterol compounds alleviated the inflammatory reaction in LPS-induced macrophage models; cell phagocytosis, nitric oxide (NO) production, release of tumor necrosis factor-α (TNF-α), and expression and activity of pro-inflammatory mediator cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and phosphorylated extracellular signal-regulated protein kinase (p-ERK) were all inhibited. The anti-inflammatory activity of β-sitosterol was higher than stigmasterol and campesterol, which suggests that phytosterols without a double bond on C-22 and with ethyl on C-24 were more effective. However, inconsistent results were observed upon comparison of ergosterol and ergosterol acetate (hydroxy or ester group on C-3), which suggest that additional research is still needed to ascertain the contribution of structure to their anti-inflammatory effects.

scholarly journals Enhancement of the Anti-Inflammatory Effect of Mustard Kimchi on RAW 264.7 Macrophages by the Lactobacillus plantarum Fermentation-Mediated Generation of Phenolic Compound Derivatives

Foods ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 181 ◽  
Author(s):  
Bao Le ◽  
Pham Anh ◽  
Seung Yang
Keyword(s):  
Nitric Oxide ◽  
Mass Spectrometry ◽  
Lactobacillus Plantarum ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Phenolic Profiles ◽  
Anti Inflammatory ◽  
Underlying Mechanisms ◽  
Factor Α ◽  
Oxide Synthase

Mustard leaf kimchi contains numerous functional compounds that have various health benefits. However, the underlying mechanisms of their anti-inflammatory effects are unclear. In this study, changes in the mustard leaf kimchi phenolics profile after fermentation with or without Lactobacillus plantarum were determined using liquid chromatography–mass spectrometry/mass spectrometry (LC–MS/MS). To correlate changes in phenolic profiles with anti-inflammatory activities of the fermentation extracts, lipopolysaccharides (LPS)-stimulated RAW 264.7 cells were treated with the extracts. We identified 12 phenolic acids in mustard leaf kimchi fermented with L. plantarum. Caffeic acid, chlorogenic acid, epicatechin, and catechin substituted the metabolite abundance. Extracts of mustard leaf kimchi fermented by L. plantarum (MLKL) markedly inhibited nitric oxide production by decreasing interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), and cyclooxygenase 2 (COX2) expression levels in LPS-treated RAW 264.7 cells. Thus, fermentation with L. plantarum potentially improves the anti-inflammatory activities of mustard leaf and mustard leaf fermented with this microorganism may serve as a proper diet for the treatment of inflammation.

scholarly journals Differential and paradoxical roles of new-generation antidepressants in primary astrocytic inflammation

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Jia-Hui He ◽  
Rong-Pei Liu ◽  
Yi-Man Peng ◽  
Qing Guo ◽  
Lan-Bing Zhu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Inflammatory Responses ◽  
Interleukin 1Α ◽  
Underlying Mechanisms ◽  
Factor Α ◽  
And Function ◽  
New Generation ◽  
Oxide Synthase ◽  
Necrosis Factor

Abstract Background Selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) are commonly used new-generation drugs for depression. Depressive symptoms are thought to be closely related to neuroinflammation. In this study, we used up-to-date protocols of culture and stimulation and aimed to understand how astrocytes respond to the antidepressants. Methods Primary astrocytes were isolated and cultured using neurobasal-based serum-free medium. The cells were treated with a cytokine mixture comprising complement component 1q, tumor necrosis factor α, and interleukin 1α with or without pretreatments of antidepressants. Cell viability, phenotypes, inflammatory responses, and the underlying mechanisms were analyzed. Results All the SSRIs, including paroxetine, fluoxetine, sertraline, citalopram, and fluvoxamine, show a visible cytotoxicity within the range of applied doses, and a paradoxical effect on astrocytic inflammatory responses as manifested by the promotion of inducible nitric oxide synthase (iNOS) and/or nitric oxide (NO) and the inhibition of interleukin 6 (IL-6) and/or interleukin 1β (IL-1β). The SNRI venlafaxine was the least toxic to astrocytes and inhibited the production of IL-6 and IL-1β but with no impact on iNOS and NO. All the drugs had no regulation on the polarization of astrocytic A1 and A2 types. Mechanisms associated with the antidepressants in astrocytic inflammation route via inhibition of JNK1 activation and STAT3 basal activity. Conclusions The study demonstrated that the antidepressants possess differential cytotoxicity to astrocytes and function differently, also paradoxically for the SSRIs, to astrocytic inflammation. Our results provide novel pieces into understanding the differential efficacy and tolerability of the antidepressants in treating patients in the context of astrocytes.

scholarly journals Differential and paradoxical roles of new-generation antidepressants in primary astrocytic inflammation

2020 ◽  
Author(s):  
Jia-Hui He ◽  
Rong-Pei Liu ◽  
Yi-Man Peng ◽  
Qing Guo ◽  
Lan-Bing Zhu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Inflammatory Responses ◽  
Interleukin 1Α ◽  
Underlying Mechanisms ◽  
Factor Α ◽  
And Function ◽  
New Generation ◽  
Oxide Synthase ◽  
Necrosis Factor

Abstract Background: Selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) are commonly used new-generation drugs for depression. Depressive symptoms are thought to be closely related to neuroinflammation. In this study, we used up-to-date protocols of culture and stimulation and aimed to understand how astrocytes respond to the antidepressants. Methods: Primary astrocytes were isolated and cultured using neurobasal-based serum free medium. The cells were treated with a cytokine mixture comprising complement component 1q, tumor necrosis factor α and interleukin 1α with or without pretreatments of antidepressants. Cell viability, phenotypes, inflammatory responses and the underlying mechanisms were analyzed. Results: All the SSRIs, including paroxetine, fluoxetine, sertraline, citalopram, and fluvoxamine, show a visible cytotoxicity within the range of applied doses, and a paradoxical effect on astrocytic inflammatory responses as manifested by the promotion of inducible nitric oxide synthase (iNOS) and/or nitric oxide (NO) and the inhibition of interleukin 6 (IL-6) and/or interleukin 1β (IL-1β). The SNRI venlafaxine was the least toxic to astrocytes and inhibited the production of IL-6 and IL-1β but with no impact on iNOS and NO. All the drugs had no regulation on the polarization of astrocytic A1 and A2 types. Mechanisms associated with the antidepressants in astrocytic inflammation route via inhibition of JNK1 activation and STAT3 basal activity. Conclusions: The study demonstrated that the antidepressants possess differential cytotoxicity to astrocytes and function differently, also paradoxically for the SSRIs, to astrocytic inflammation. Our results provide novel pieces into understanding the differential efficacy and tolerability of the antidepressants in treating patients in the context of astrocytes.

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

Molecules ◽  
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.

scholarly journals MiR-155/GSK-3β mediates anti-inflammatory effect of Chikusetsusaponin IVa by inhibiting NF-κB signaling pathway in LPS-induced RAW264.7 cell

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yi Xin ◽  
Qin Yuan ◽  
Chaoqi Liu ◽  
Changcheng Zhang ◽  
Ding Yuan
Keyword(s):  
Signaling Pathway ◽  
Mouse Liver ◽  
Inflammatory Responses ◽  
Biological Activities ◽  
Raw264.7 Cells ◽  
Inflammation Model ◽  
Raw264.7 Cell ◽  
Anti Inflammatory ◽  
Gsk 3Β ◽  
Inflammatory Effect

Abstract It has been demonstrated that Chikusetsusaponin IVa (CsIVa) possesses abundant biological activities. Herein, using LPS to establish acute inflammation model of mouse liver and cell line inflammation model, we investigated whether miR-155/GSK-3β regulated NF-κB signaling pathway, and CsIVa exerted anti-inflammatory effects by regulating miR-155/GSK-3β signaling pathway. Our results showed that LPS induced high expression of miR-155 and miR-155 promoted macrophage activation through GSK-3β. In addition, CsIVa inhibited inflammatory responses in LPS-induced mouse liver and RAW264.7 cells. Furthermore, we demonstrated that CsIVa improved the inflammatory response in LPS-induced RAW264.7 cells by inhibiting miR-155, increasing GSK-3β expression, and inhibiting NF-κB signaling pathway. In conclusion, our study reveals that CsIVa suppresses LPS-triggered immune response by miR-155/GSK-3β-NF-κB signaling pathway.

scholarly journals Effect of Kramecyne on the Inflammatory Response in Lipopolysaccharide-Stimulated Peritoneal Macrophages

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
E. Sánchez-Miranda ◽  
J. Lemus-Bautista ◽  
S. Pérez ◽  
J. Pérez-Ramos
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Peritoneal Macrophages ◽  
Anti Inflammatory ◽  
Oxide Synthase ◽  
North And South America ◽  
North And South ◽  
Mouse Peritoneal Macrophages ◽  
Necrosis Factor

Kramecyne is a new peroxide, it was isolated fromKrameria cytisoides, methanol extract, and this plant was mostly found in North and South America. This compound showed potent anti-inflammatory activity; however, the mechanisms by which this compound exerts its anti-inflammatory effect are not well understood. In this study, we examined the effects of kramecyne on inflammatory responses in mouse lipopolysaccharide- (LPS-) induced peritoneal macrophages. Our findings indicate that kramecyne inhibits LPS-induced production of tumor necrosis factor (TNF-α) and interleukin- (IL-) 6. During the inflammatory process, levels of cyclooxygenase- (COX-) 2, nitric oxide synthase (iNOS), and nitric oxide (NO) increased in mouse peritoneal macrophages; however, kramecyne suppressed them significantly. These results provide novel insights into the anti-inflammatory actions and support its potential use in the treatment of inflammatory diseases.

scholarly journals Kuwanon T and Sanggenon a Isolated from Morus alba Exert Anti-Inflammatory Effects by Regulating NF-κB and HO-1/Nrf2 Signaling Pathways in BV2 and RAW264.7 Cells

Molecules ◽  
2021 ◽  
Vol 26 (24) ◽  
pp. 7642
Author(s):  
Wonmin Ko ◽  
Zhiming Liu ◽  
Kwan-Woo Kim ◽  
Linsha Dong ◽  
Hwan Lee ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Diseases ◽  
Cell Types ◽  
Morus Alba ◽  
Related Factor ◽  
Nuclear Factor ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor

We previously investigated the methanolic extract of Morus alba bark and characterized 11 compounds from the extract: kuwanon G (1), kuwanon E (2), kuwanon T (3), sanggenon A (4), sanggenon M (5), sanggenol A (6), mulberofuran B (7), mulberofuran G (8), moracin M (9), moracin O (10), and norartocarpanone (11). Herein, we investigated the anti-inflammatory effects of these compounds on microglial cells (BV2) and macrophages (RAW264.7). Among them, 3 and 4 markedly inhibited the lipopolysaccharide (LPS)-induced production of nitric oxide in these cells, suggesting the anti-inflammatory properties of these two compounds. These compounds inhibited the production of prostaglandin E2, interleukin-6, and tumor necrosis factor-α, and the expression of inducible nitric oxide synthase and cyclooxygenase-2 following LPS stimulation. Pretreatment with 3 and 4 inhibited the activation of the nuclear factor kappa B signaling pathway in both cell types. The compounds also induced the expression of heme oxygenase (HO)-1 through the activation of nuclear factor erythroid 2-related factor 2. Suppressing the activity of HO-1 reversed the anti-inflammatory effects caused by pretreatment with 3 and 4, suggesting that the anti-inflammatory effects were regulated by HO-1. Taken together, 3 and 4 are potential candidates for developing therapeutic and preventive agents for inflammatory diseases.

scholarly journals Cnicin from Centaurea benedicta L. is an active compound against skin inflammation in a mouse model

2021 ◽  
Author(s):  
Orlando Vieira Sousa ◽  
Guilherme C. Gonçalves ◽  
Lucas S. Queiroz ◽  
Everton A. Ferreira ◽  
Bruna C. S. Santos ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mouse Model ◽  
Skin Inflammation ◽  
Cyclooxygenase 1 ◽  
Tnf Α ◽  
Inflammatory Processes ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase

Abstract Centaurea benedicta L., commonly known as “cardo santo,” is used as a tonic, antidepressant, anti-inflammatory, antibacterial, and antiseptic in traditional medicine. This study evaluated the topical anti-inflammatory potential of an extract (ECB) and cnicin (CNI) from C. benedicta leaves in a mouse model. Activity was assessed using the ear edema method with croton oil, phenol, capsaicin, and histamine as phlogistic agents. Myeloperoxidase (MPO), N-acetyl-β-D-glucosaminidase (NAG), nitric oxide (NO), t umor necrosis factor α (TNF-α), interleukin 6 (IL-6), and histopathology were assessed as markers of edema/inflammation. Interaction profiles between CNI and cyclooxygenase-1 and -2, induced nitric oxide synthase, and glucocorticoid receptor were examined with molecular docking. Twenty-four h after induction of inflammation, ECB and CNI treatments decreased the thickness and weight of ears by 39.59%– 94.72%. MPO, NAG, NO, TNF-α, and IL-6 levels were also reduced. Histopathological, treatments reduced edema thickness, leukocytes, and vasodilation. Inflammation induced by phenol and histamine was inhibited by ECB and CNI, and ECB suppressed capsaicin-induced inflammation. CNI interacts with cyclooxygenase-1 and nitric oxide synthase through conventional hydrogen bonds, indicating inhibition of these enzymes. ECB and its compound cnicin reduce chemically-induced inflammation in mice suggesting new possibilities for the treatment of diseases associated with dermal inflammatory processes.

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