scholarly journals Chlorogenic Acid Attenuates Oxidative Stress-Induced Intestinal Epithelium Injury by Co-Regulating the PI3K/Akt and IκBαNF-κB Signaling

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1915
Author(s):  
Jiali Chen ◽  
Yuheng Luo ◽  
Yan Li ◽  
Daiwen Chen ◽  
Bing Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chlorogenic Acid ◽  
Intestinal Epithelium ◽  
Heme Oxygenase 1 ◽  
Signaling Proteins ◽  
Nuclear Factor ◽  
Specific Inhibition ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Inflammatory Effect

Chlorogenic acid (CGA) is a natural polyphenol compound abundant in green plants with antioxidant and anti-inflammatory activities. Here, we explore its protective effects and potential mechanisms of action on intestinal epithelium exposure to oxidative stress (OS). We show that CGA attenuated OS-induced intestinal inflammation and injury in weaned pigs, which is associated with elevated antioxidant capacity and decreases in inflammatory cytokine secretion and cell apoptosis. In vitro study showed that CGA elevated phosphorylation of two critical signaling proteins of the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) pathway, Akt and nuclear factor erythroid-derived-related factor 2, leading to the elevated expression of intracellular antioxidant enzymes and heme oxygenase-1 (HO-1). Specific inhibition of HO-1 partially abolished its anti-inflammatory effect in IPEC-J2 cells exposure to OS. Interestingly, CGA suppressed the tumor necrosis factor-α (TNF-α) induced inflammatory responses in IPEC-J2 cells by decreasing phosphorylation of two critical inflammatory signaling proteins, NF-kappa-B inhibitor alpha (IκBα) and nuclear factor-κB (NF-κB). Specific inhibition of HO-1 cannot fully abolish its anti-inflammatory effect on the TNF-α-challenged cells. These results strongly suggested that CGA is a natural anti-inflammatory agent that can attenuate OS-induced inflammation and injury of intestinal epithelium via co-regulating the PI3K/Akt and IκBα/NF-κB signaling pathway.

scholarly journals (–)-Loliolide Isolated from Sargassum horneri Suppressed Oxidative Stress and Inflammation by Activating Nrf2/HO-1 Signaling in IFN-γ/TNF-α-Stimulated HaCaT Keratinocytes

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 856
Author(s):  
Eui-Jeong Han ◽  
Ilekuttige Priyan Shanura Fernando ◽  
Hyun-Soo Kim ◽  
Dae-Sung Lee ◽  
Areum Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nuclear Factor Κb ◽  
Sargassum Horneri ◽  
Mitogen Activated Protein Kinase ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Nuclear Factor ◽  
Hacat Keratinocytes ◽  
Tnf Α ◽  
Ifn Γ

The present study evaluated the effects of (–)-loliolide isolated from Sargassum horneri (S. horneri) against oxidative stress and inflammation, and its biological mechanism in interferon (IFN)-γ/tumor necrosis factor (TNF)-α-stimulated HaCaT keratinocytes. The results showed that (–)-loliolide improved the cell viability by reducing the production of intracellular reactive oxygen species (ROS) in IFN-γ/TNF-α-stimulated HaCaT keratinocytes. In addition, (–)-loliolide effectively decreased the expression of inflammatory cytokines (interleukin (IL)-4 IL-6, IL-13, IFN-γ and TNF-α) and chemokines (CCL11 (Eotaxin), macrophage-derived chemokine (MDC), regulated on activation, normal T cell expressed and secreted (RANTES), and thymus and activation-regulated chemokine (TARC)), by downregulating the expression of epidermal-derived initial cytokines (IL-25, IL-33 and thymic stromal lymphopoietin (TSLP)). Furthermore, (–)-loliolide suppressed the activation of mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) signaling, whereas it activated nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling. Interestingly, the cytoprotective effects of (–)-loliolide against IFN-γ/TNF-α stimulation were significantly blocked upon inhibition of HO-1. Taken together, these results suggest that (–)-loliolide effectively suppressed the oxidative stress and inflammation by activating the Nrf2/HO-1 signaling in IFN-γ/TNF-α-stimulated HaCaT keratinocytes.

scholarly journals Alpha-Linolenic Acid Impedes Cadmium-Induced Oxidative Stress, Neuroinflammation, and Neurodegeneration in Mouse Brain

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2274
Author(s):  
Sayed-Ibrar Alam ◽  
Min-Woo Kim ◽  
Fawad Ali Shah ◽  
Kamran Saeed ◽  
Rahat Ullah ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Linolenic Acid ◽  
Mouse Brain ◽  
Neuronal Apoptosis ◽  
Neuroprotective Effect ◽  
Heme Oxygenase 1 ◽  
Nuclear Factor ◽  
Alpha Linolenic Acid ◽  
Antioxidant Agents ◽  
Anti Inflammatory

Alpha-Linolenic acid (ALA), an omega-3 polyunsaturated fatty acid, is extracted from plant sources and has been shown to be one of the anti-inflammatory and antioxidant agents. Herein, we revealed the molecular mechanism underlying the anti-inflammatory and antioxidant potential of (ALA), against cadmium in the adult mouse brain. We evaluated the neuroprotective effect of ALA (60 mg/kg per oral for 6 weeks) against CdCl2 (5 mg/kg)-induced oxidative stress, neuroinflammation, and neuronal apoptosis. According to our findings, ALA markedly reduced ROS production and nitric oxide synthase 2 (NOS2) and enhanced the expression of nuclear factor-2 erythroid-2 (Nrf-2) and heme oxygenase-1 (HO-1) in mice treated with CdCl2. Most importantly, the molecular docking study revealed that ALA allosterically decreases the overexpression of c-Jun N-terminal kinase (JNK) activity and inhibited the detrimental effect against CdCl2. Moreover, ALA suppressed CdCl2-induced glial fibrillary acidic protein (GFAP), nuclear factor-kappa b (NF-κB), and interleukin-1β (IL-1β) in the mouse brain. Further, we also checked the pro- and anti-apoptotic proteins markers such as Bax, Bcl-2, and caspase-3, which were regulated in the cortex of ALA co-treated mouse brain. Overall, our study suggests that oral administration of ALA can impede oxidative stress, neuroinflammation, and increase neuronal apoptosis in the cortex of Cd-injected mouse brain.

scholarly journals Rice Protein Exerts Anti-Inflammatory Effect in Growing and Adult Rats via Suppressing NF-κB Pathway

2019 ◽  
Vol 20 (24) ◽  
pp. 6164
Author(s):  
Zhengxuan Wang ◽  
Mingcai Liang ◽  
Hui Li ◽  
Liang Cai ◽  
Lin Yang
Keyword(s):  
Nuclear Factor Κb ◽  
Interleukin 10 ◽  
Heme Oxygenase 1 ◽  
Mrna Levels ◽  
Nuclear Factor ◽  
Adult Rats ◽  
Monocyte Chemoattractant Protein 1 ◽  
Rice Protein ◽  
Anti Inflammatory ◽  
Inflammatory Effect

To elucidate the effect of rice protein (RP) on the depression of inflammation, growing and adult rats were fed with caseins and RP for 2 weeks. Compared with casein, RP reduced hepatic accumulations of reactive oxygen species (ROS) and nitro oxide (NO), and plasma activities of alanine transaminase (ALT) and aspartate transaminase (AST) in growing and adult rats. Intake of RP led to increased mRNA levels, and protein expressions of phosphoinositide 3 kinase (PI3K), protein kinase B (Akt), nuclear factor-κB 1 (NF-αB1), reticuloendotheliosis viral oncogene homolog A (RelA), tumor necrotic factor α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and monocyte chemoattractant protein-1 (MCP-1) were decreased, whereas hepatic expressions of interleukin-10 (IL-10) and heme oxygenase 1 (HO-1) were increased by RP. The activation of NF-κB was suppressed by RP through upregulation of inhibitory κB α (IκBα), resulting in decreased translocation of nuclear factor-κB 1 (p50) and RelA (p65) to the nucleus in RP groups. The present study demonstrates that RP exerts an anti-inflammatory effect to inhibit ROS-derived inflammation through suppression of the NF-κB pathway in growing and adult rats. Results suggest that the anti-inflammatory capacity of RP is independent of age.

scholarly journals Anti-Inflammatory Effects of Ribes diacanthum Pall Mediated via Regulation of Nrf2/HO-1 and NF-κB Signaling Pathways in LPS-Stimulated RAW 264.7 Macrophages and a TPA-Induced Dermatitis Animal Model

Antioxidants ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 622
Author(s):  
Na Yeon Kim ◽  
Sun Hee Cheong ◽  
Kun Jong Lee ◽  
Dai-Eun Sok ◽  
Mee Ree Kim
Keyword(s):  
Nitric Oxide ◽  
Animal Model ◽  
Nuclear Translocation ◽  
Raw 264.7 Cells ◽  
Heme Oxygenase 1 ◽  
Raw 264.7 ◽  
Nuclear Factor ◽  
Raw 264.7 Macrophages ◽  
Tnf Α ◽  
Anti Inflammatory

Ribes diacanthum Pall (RDP) is a Mongolian traditional medicine used to treat renal inflammation. In the present study, we initially investigated the anti-inflammatory effects and mechanisms of action of ethylacetate extract of RDP (EARDP) in RAW 264.7 macrophages stimulated by lipopolysaccharide (LPS) and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced dermatitis in mice. We demonstrated that EARDP protected against LPS-induced cell death by inhibiting intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) production, as well as the synthesis of pro-inflammatory mediators and cytokines, such as nitric oxide (NO), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and IL-1β. EARDP inhibited the phosphorylation and degradation of inhibitory κB-α (IκB-α) and the activation of nuclear factor (NF)-κB, indicating that the anti-inflammatory effect of EARDP was mediated via the suppression of NF-κB nuclear translocation. In addition, EARDP induced the heme oxygenase-1 (HO-1) expression and nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2), indicating that EARDP induced HO-1 via the Nrf2 pathway in RAW 264.7 cells. Furthermore, EARDP significantly suppressed the protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in LPS-stimulated RAW 264.7 macrophages. However, ZnPP, a specific inhibitor of HO-1, reversed the EARDP-mediated inhibition of NO and TNF-α production in LPS-stimulated RAW 264.7 macrophages. EARDP blocked the phosphorylation of mitogen-activated protein kinase (MAPK) and Akt in LPS-stimulated RAW 264.7 cells. In the in vivo animal model, EARDP significantly and dose-dependently reduced TPA-induced secretion of TNF-α and IL-6 in mouse ear. Based on these results, EARDP represents a promising natural compound, protective against oxidative stress and inflammatory diseases.

scholarly journals Induction of Heme Oxygenase-1 by Sodium 9-Hydroxyltanshinone IIA Sulfonate Derivative Contributes to Inhibit LPS-Mediated Inflammatory Response in Macrophages

2015 ◽  
Vol 36 (4) ◽  
pp. 1316-1330 ◽  
Author(s):  
Xin-Hua Liu ◽  
Xi-Ling Wang ◽  
Hong Xin ◽  
Dan Wu ◽  
Xiao-Ming Xin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Response ◽  
Heme Oxygenase ◽  
Inos Expression ◽  
Heme Oxygenase 1 ◽  
Zinc Protoporphyrin ◽  
Nuclear Factor ◽  
Anti Inflammatory ◽  
Underlying Mechanisms ◽  
Inflammatory Effect

Background/Aim: Sodium 9-acetoxyltanshinone IIA sulfonate (ZY-1A4), a novel compound derived from sodium 9-hydroxyltanshinone IIA sulfonate, was synthesized with potential biological activities. This study aimed to explore the effects of ZY-1A4 on lipopolysaccharide (LPS)-triggered inflammatory response and the underlying mechanisms. Methods: Activation of RAW264.7 macrophages was induced by LPS. The effects of ZY-1A4 on inducible nitric oxide synthase (iNOS) expression, nitric oxide (NO) generation, nuclear factor-κB (NF-κB) activation, heme oxygenase-1 (HO-1) expression, and nuclear factor-erythroid 2 related factor 2 (Nrf2) pathway were evaluated to elucidate its underlying mechanisms on inflammatory responses. Results: ZY-1A4 concentration-dependently reduced iNOS expression and NO production, and inhibited c-Jun-N-terminal kinase 1/2 (JNK1/2) phosphorylation and NF-κB activation in LPS-stimulated macrophages. In addition, ZY-1A4 concentration- and time-dependently induced HO-1 expression associated with degradation of Kelch-like ECH-associated protein 1 (Keap1) and nuclear translocation of Nrf2, while the effect of ZY-1A4 was abolished by a phosphoinositide 3-kinase (PI3K) inhibitor LY294002. Intriguingly, pharmacological inactivation of HO-1 with zinc protoporphyrin IX reversed anti-inflammatory effect of ZY-1A4, but the anti-inflammatory effect of ZY-1A4 was largely mimicked by HO-1 by-products carbon monoxide and bilirubin. Furthermore, the inhibitory effect of ZY-1A4 on LPS-induced iNOS expression and NO release was abolished by HO-1 siRNA or LY294002. Conclusion: Our results demonstrated that ZY-1A4 suppressed LPS-induced iNOS expression and NO generation via modulation of NF-κB activation and HO-1 expression. This new finding might shed light to the prevention and therapy of cardiovascular diseases.

scholarly journals Anti-Inflammatory Properties, Bioaccessibility and Intestinal Absorption of Sea Fennel (Crithmum maritimum) Extract Encapsulated in Soy Phosphatidylcholine Liposomes

Nutrients ◽  
2022 ◽  
Vol 14 (1) ◽  
pp. 210
Author(s):  
Ailén Alemán ◽  
Daniel Marín-Peñalver ◽  
Pilar Fernández de Palencia ◽  
María del Carmen Gómez-Guillén ◽  
Pilar Montero
Keyword(s):  
Chlorogenic Acid ◽  
Cell Monolayer ◽  
Inflammatory Activity ◽  
Polyphenolic Compound ◽  
Gastrointestinal Digestion ◽  
Phosphatidylcholine Liposomes ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Inflammatory Effect

A sea fennel (Crithmum maritimum) aqueous extract was prepared and loaded into soybean phosphatidylcholine liposomes. Both the free extract (FE), and the empty (L) and loaded (L-FE) liposomes were shown to be non-cytotoxic to THP-1 and Caco-2 cells. The anti-inflammatory effect was tested on THP-1 cells differentiated into macrophages. FE showed anti-inflammatory activity, revealed by the induced secretion of IL-10 cytokines in macrophages that were subsequently stimulated with LPS. Also, a decrease in TNF-α production by L was observed, evidencing that liposomes reduced the pro-inflammatory mediators’ secretion. The liposomes (L) showed protective anti-inflammatory activity and also were able to downregulate the inflammation. Furthermore, L-FE were also found to downregulate the inflammation response, as they were able to decrease TNF-α secretion in macrophages previously exposed to LPS. The simulated in vitro gastrointestinal digestion (GID) of FE diminished the chlorogenic acid content (the main polyphenolic compound of the extract) by 40%, while in L-FE, the amount of this phenolic compound increased with respect to the undigested liposomes. The amount of bioaccessible chlorogenic, however, was similar for FE and L-FE. The percentage of chlorogenic acid absorbed through a Caco-2 cell monolayer after 3 h of incubation, was significantly similar for the extract and the liposomes (~1.5%), without finding significant differences once the extract and liposomes were digested.

Anti-Inflammatory Effect of Dohongsamultang through Inhibition of Nuclear Factor-κB Activation in Peripheral Blood Mononuclear Cells of Patients with Cerebral Infarction

2007 ◽  
Vol 35 (03) ◽  
pp. 415-426 ◽  
Author(s):  
Su-Jin Kim ◽  
Hyun-Ja Jeong ◽  
Sei-Uk Park ◽  
Byung-Soon Moon ◽  
Phil-Dong Moon ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Mononuclear Cells ◽  
Dependent Manner ◽  
Nuclear Factor ◽  
Peripheral Blood Mononuclear ◽  
Inflammatory Reactions ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Dose Dependent ◽  
Inflammatory Effect

The Korean indigenous medicine "Dohongsamultang (DHSMT)" has long been used for various cerebrovascular diseases. However, the exact mechanism for the anti-inflammatory effect of DHSMT is not completely understood. The aim of the present study is to elucidate how DHSMT modulates the inflammatory reaction in lipopolysaccaride (LPS)-stimulated peripheral mononuclear cells from cerebral infarction (CI) patients. Production and expression of cytokine was measured via the ELISA and RT-PCR methods. The level of nuclear factor-kappa B (NF-κB)/Rel A protein and NF-κB DNA binding activity were determined via the Western blot analysis and transcription factor enzyme-linked immunoassay. It showed that DHSMT inhibited the production of TNF-α, IL-1β, and IL-6 induced by LPS in a dose-dependent manner ( p < 0.05). The maximal inhibition rates for TNF-α, IL-1β, and IL-6 production by DHSMT were about 50.18%, 32.13%, and 38.03%, respectively. DHSMT inhibited the TNF-α mRNA expression in a dose-dependent manner. We also showed that the inhibitory effect of DHSMT is through the suppression of the NF-κB pathway. The study suggests an important molecular mechanism by GMGHT to reduce inflammation, which might explain its beneficial effect in the regulation of inflammatory reactions.

scholarly journals Sargachromenol Purified from Sargassum horneri Inhibits Inflammatory Responses via Activation of Nrf2/HO-1 Signaling in LPS-Stimulated Macrophages

Marine Drugs ◽  
2021 ◽  
Vol 19 (9) ◽  
pp. 497
Author(s):  
Eui-Jeong Han ◽  
Thilina U. Jayawardena ◽  
Jae-Hyuk Jang ◽  
Ilekuttige Priyan Shanura Fernando ◽  
Youngheun Jee ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Mapk Signaling ◽  
Sargassum Horneri ◽  
Heme Oxygenase 1 ◽  
Raw 264.7 ◽  
Related Factor ◽  
Nuclear Factor ◽  
Raw 264.7 Macrophages ◽  
Anti Inflammatory ◽  
Inflammatory Effect

In this study, we isolated sargachromenol (SC) from Sargassum horneri and evaluated its anti-inflammatory effect in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. SC did not show cytotoxicity at all concentrations and effectively increased the cell viability by reducing the nitric oxide (NO) and intracellular reactive oxygen species (ROS) production in LPS-stimulated RAW 264.7 macrophages. In addition, SC decreased the mRNA expression levels of inflammatory cytokines (IL-1β, IL-6, and TNF-α) and inflammatory mediators (iNOS and COX-2). Moreover, SC suppressed the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) and mitogen-activated protein kinase (MAPK) signaling, whereas activated the nuclear factor erythroid 2-related factor 2/heme oxygenase-1 (Nrf2/HO-1) signaling in LPS-stimulated RAW 264.7 macrophages. Interestingly, the anti-inflammatory effect of SC was abolished by the inhibition of HO-1 in LPS-stimulated RAW 264.7 macrophages. According to the results, this study suggests that the antioxidant capacity of SC leads to its anti-inflammatory effect and it potentially may be utilized in the nutraceutical and pharmaceutical sectors.

scholarly journals Anti-Inflammatory Effect of Ecklonia cava Extract on Porphyromonas gingivalis Lipopolysaccharide-Stimulated Macrophages and a Periodontitis Rat Model

Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 1143 ◽  
Author(s):  
Seonyoung Kim ◽  
Soo-Im Choi ◽  
Gun-Hee Kim ◽  
Jee-Young Imm
Keyword(s):  
Porphyromonas Gingivalis ◽  
Nuclear Factor Κb ◽  
Ecklonia Cava ◽  
Heme Oxygenase 1 ◽  
Therapeutic Effects ◽  
Related Factor ◽  
Nuclear Factor ◽  
Porphyromonas Gingivalis Lipopolysaccharide ◽  
Anti Inflammatory ◽  
Inflammatory Effect

Ecklonia cava, an edible marine brown alga (Laminariaceae), is a rich source of phlorotannins. This study aimed to investigate the anti-inflammatory effect of Ecklonia cava ethanol extract (ECE, dieckol 10.6%, w/w) on Porphyromonas gingivalis lipopolysaccharide-stimulated inflammation in RAW 264.7 cells and in ligature-induced periodontitis in rats. The levels of nitric oxide (NO) and prostaglandin E2 were decreased by more than half on treatment with 100 μg/mL ECE. Downregulated tumor necrosis factor-α, interleukin (IL)-1β, and IL-6 gene expression confirmed the anti-inflammatory properties of ECE. ECE treatment upregulated heme oxygenase-1 (HO-1) expression by 6.3-fold and increased HO-1/nuclear factor erythroid 2-related factor 2 (Nrf-2) signaling decreased nuclear factor-κB (NF-κB) translocation. ECE administration (400 mg/kg) significantly reduced gingival index, restricted tooth mobility, and prevented alveolar bone loss (p < 0.05). These beneficial effects were due to decreased inflammatory cell infiltration, IL-1β production, and matrix metalloproteinase expression in gingival tissues. The ratio of receptor activator of nuclear factor-κB ligand (RANKL)/osteoprotegerin, a biomarker of periodontitis and osteolysis, was significantly decreased by ECE administration (p < 0.05). Thus, ECE has potential therapeutic effects for the alleviation of periodontal disease.

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