Suppression of LPS-Induced Hepato- and Cardiotoxic Effects by Pulicaria petiolaris via NF-κB Dependent Mechanism

Ahmed, Naseer; El‐Agamy, Dina S.; Mohammed, Gamal; Abo‐Haded, Hany M.; Elkablawy, Mohamed A.; Ibrahim, Sabrin R. M.

doi:10.1007/s12012-019-09539-4

Cited by 16 publications

(14 citation statements)

References 35 publications

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“…15,16 In terms of oxidative stress, the catalytic subunit gp91phox (NOX2) of triphosphopyridine nucleotide (NADPH) oxidase and its homologs NOX1, NOX3, NOX4, NOX5, DUOX1, and DUOX2 are collectively referred to as the NOX family. 17 These core subunits are key for the function of NADPH oxidase. 18 As a signal molecule, reactive oxygen species (ROS) produced by NADPH oxidase in nonphagocytic cells participate in the signal transduction pathway and regulate cell differentiation, proliferation, aging, and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Effect of roasted peanut allergen Ara h 3 protein on the sensitization of Caco‐2 cells

et al. 2021

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BACKGROUND: Roasted peanut is widely loved as a kind of food with rich taste. However, peanut allergy is one of the major threats to human health, which affects about 5% of children and 1.4-2% of adults in the world. RESULTS: To evaluate the sensitization mechanism of peanut allergen Ara h 3, Caco-2 cells as the model, which has the similar structure and function to differentiated small intestinal epithelial cells. Compared with Ara h 3-raw (purified from raw peanut) group, more significant results such as the inhibited Caco-2 cell viability and proliferation, the increased secretion of reactive oxygen species (ROS) and the decreased transepithelial electrical resistance were obtained in Ara h 3-roasted (purified from roasted peanut) group. Accordingly, oxidative stress and NF-κB signaling pathway were more imbalanced, which lead to the increased of thymic stromal lymphopoietin (TSLP), interleukin 6 (IL-6), IL-8 and monocyte chemotactic protein 1 (MCP-1). Then, the gene expression of tight junction proteins ZO-1, occludin and JAM-1 were reduced, which proved that the integrity of the Caco-2 monolayer barrier is severely damaged.CONCLUSION: These finding identify the mechanisms of the allergenicity of roasted peanut allergy proteins are probably associated with intestinal uptake and cytokine dependent allergies. The aggravated allergic reaction might be caused by the increment of TSLP, IL-6, IL-8 and MCP-1 due to the activated NF-κB signaling pathway, and the enhanced transport of Ara h 3-roasted protein by Caco-2 monolayer.

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Section: Introductionmentioning

confidence: 99%

Effect of roasted peanut allergen Ara h 3 protein on the sensitization of Caco‐2 cells

et al. 2021

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“…We hypothesized that accumulation of LPS can activate the TLR4/NF-κB signaling pathway through combination of TLR4 in hepatic cells, thereby regulating NF-κB-dependent liver acute and chronic inflammatory damage. To date, however, no relevant research has been carried out[ 16 - 18 ].…”

Section: Introductionmentioning

confidence: 99%

Novel roles of lipopolysaccharide and TLR4/NF-κB signaling pathway in inflammatory response to liver injury in Budd-Chiari syndrome

Li¹,

Chen²,

Zhou³

et al. 2021

WJGS

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BACKGROUND Budd-Chiari syndrome (BCS) is an uncommon disorder characterized by obstruction of hepatic venous outflow. To date, the exact mechanism underlying hepatic injury derived from the hepatic venous outflow obstruction in BCS remains largely unknown. AIM To assess the role of NF-κB-mediated inflammation in BCS-induced liver injury in humans and rats. METHODS A total of 180 rats were randomly assigned into nine groups, including four BCS model groups (1, 3, 6 and 12 wk), four sham-operated groups (1, 3, 6 and 12 wk), and a control group. Lipopolysaccharide (LPS) levels in each group were detected by the Tachypleus Amebocyte Lysate assay. The mRNA and protein levels of TLR4, NF-κB, tumor necrosis factor (TNF)-α, interleukin (IL)-2 and interferon (IFN)-γ were quantified. In addition, 60 patients with BCS and 30 healthy controls were enrolled, and their blood samples were analyzed. RESULTS Hepatic and plasma LPS levels were significantly increased in rats. The mRNA and protein expression levels of TLR4, NF-κB and inflammatory cytokines (TNF-α, IL-2 and IFN-γ) in liver tissues were significantly higher in the BCS model groups compared with the other two groups. In addition, the model groups (1, 3, 6 and 12 wk after BCS induction) showed significant differences in the levels of LPS, TLR4, NF-κB, TNF-α, IL-2 and IFN-γ. Notably, there was a significant correlation between the LPS concentrations and mRNA and protein levels of TLR4, NF-κB and inflammatory cytokines. Importantly, it was revealed that the levels of LPS, TLR4, NF-κB and inflammatory cytokines were significantly greater in chronic BCS patients than healthy controls and acute BCS patients. CONCLUSION LPS level is markedly elevated in BCS, in turn activating the TLR4/NF-κB signaling pathway, leading to induction of inflammatory cytokines (TNF-α, IL-2 and IFN-γ) in response to BCS-induced liver injury.

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“…Cytokines have been suggested to be responsible for endotoxinmediated myocardial injury 8,9 . Increased myocardial and serum levels of TNF-α and IL-6 during Lps-mediated systemic inflammatory responses have shown to be associated with both cellular and functional cardiac deterioration 10,11 . Furthermore, inhibition of TNF-α has been observed to attenuate endotoxin induced myocardial injury 12,13 .…”

Section: ■ Introductionmentioning

confidence: 99%

TNF-alpha inhibitor adalimumab attenuates endotoxin induced cardiac damage in rats

et al. 2020

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Design of the study, acquisition and analysis of data, final approval. ORIGINAL ARTICLE Experimental SurgeryActa Cir Bras. 2020;35(2):e202000202 AbstractPurpose: To investigate the effects of adalimumab pretreatment on the lipopolysaccharide-mediated myocardial injury.Methods: Twenty-eight Wistar rats were randomized into four groups (n=7). Control (C) group animals were injected once a day with intraperitoneal (i.p) 0.9 % saline for two days. In the Adalimumab (Ada) group, adalimumab was injected at a dose of 10 mg/kg/ day (i.p) for two days. Lipopolysaccharide (Lps) group rats were injected with a dose of 5 mg/kg (i.p) lipopolysaccharide. Lipopolysaccharide + Adalimumab (Lps+Ada) group rats received adalimumab before the administration of lipopolysaccharide. The animals were sacrificed 24 h after the last injection and blood samples were obtained for determination of biochemical cardiac injury markers and circulating levels of TNF-α and interleukin-6 (IL-6). Hearts were harvested for histological examination.Results: Endotoxin exposure resulted in significant increases in serum cardiac injury markers, serum cytokines and histological myocardial injury scores in the Lps group. The levels of circulating cytokines, cardiac injury markers and histological injury scores for myocardial necrosis, perivascular cell infiltration, and inflammation were significantly reduced in Lps+Ada as compared to Lps group (p<0.05). Conclusions:Adalimumab pretreatment reduces endotoxin-induced myocardial damage in rats. This beneficial effect is thought to be related to the reduction of cytokine release.

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Suppression of LPS-Induced Hepato- and Cardiotoxic Effects by Pulicaria petiolaris via NF-κB Dependent Mechanism

Cited by 16 publications

References 35 publications

Effect of roasted peanut allergen Ara h 3 protein on the sensitization of Caco‐2 cells

Effect of roasted peanut allergen Ara h 3 protein on the sensitization of Caco‐2 cells

Novel roles of lipopolysaccharide and TLR4/NF-κB signaling pathway in inflammatory response to liver injury in Budd-Chiari syndrome

TNF-alpha inhibitor adalimumab attenuates endotoxin induced cardiac damage in rats

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