Preconditioning with L-Ala-Gln reduces the expression of inflammatory markers (TNF-α, NF-κB, IL-6 and HO-1) in an injury animal model of cerebrovascular ischemia in Meriones unguiculatus (gerbils)

Oliveira, Leidelamar Rosário Alves de; Albuquerque, Andrea de Oliveira; Silva, Cícero Igor Simões Moura; Silva, Jussara Mathiele; Casadevall, Meyssa Quezado de Figueiredo Cavalcante; Azevedo, Orleâncio Gomes Ripardo de; Albuquerque, Vilma Leite de Souza Pires; Vasconcelos, Paulo Roberto Leitão de

doi:10.1590/s0102-865020200060000001

Cited by 8 publications

(3 citation statements)

References 26 publications

(34 reference statements)

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“…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. 19 With abnormal expression of NOX family proteins, ROS levels increase sharply, which can induce a number of changes, including activation of the NF-κB signal pathway.…”

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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“…Therefore, inflammation is an important driving factor in the LPS/D-Gal-induced acute liver injury model, and it is essential to investigate whether Ala-Gln plays an anti-inflammatory role in damaged liver tissue. Gerbils that were pretreated with Ala-Gln showed a reduced expression proinflammatory factors, including TNF-α, IL-6, and NF-κB, in a model of brain ischemia–reperfusion injury [ 49 ]. A previous study showed that Ala-Gln administration significantly inhibited the production of TNF-α and TNF-α-mediated NF-κB pathway activation in skeletal muscle in hindlimb immobilization-induced disuse muscle atrophy rats [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

Alanyl-Glutamine Protects against Lipopolysaccharide-Induced Liver Injury in Mice via Alleviating Oxidative Stress, Inhibiting Inflammation, and Regulating Autophagy

Ying

Zheng

et al. 2022

Antioxidants

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Acute liver injury is a worldwide problem with a high rate of morbidity and mortality, and effective pharmacological therapies are still urgently needed. Alanyl-glutamine (Ala-Gln), a dipeptide formed from L-alanine and L-glutamine, is known as a protective compound that is involved in various tissue injuries, but there are limited reports regarding the effects of Ala-Gln in acute liver injury. This present study aimed to investigate the protective effects of Ala-Gln in lipopolysaccharide (LPS)-induced acute liver injury in mice, with a focus on inflammatory responses and oxidative stress. The acute liver injury induced using LPS (50 μg/kg) and D-galactosamine (D-Gal) (400 mg/kg) stimulation in mice was significantly attenuated after Ala-Gln treatment (500 and 1500 mg/kg), as evidenced by reduced plasma alanine transaminase (ALT) (p < 0.01, p < 0.001), aspartate transaminase (AST) (p < 0.05, p < 0.001), and lactate dehydrogenase (LDH) (p < 0.01, p < 0.001) levels, and accompanied by improved histopathological changes. In addition, LPS/D-Gal-induced hepatic apoptosis was also alleviated by Ala-Gln administration, as shown by a greatly decreased ratio of TUNEL-positive hepatocytes, from approximately 10% to 2%, and markedly reduced protein levels of cleaved caspase-3 (p < 0.05, p < 0.001) in liver. Moreover, we found that LPS/D-Gal-triggered oxidative stress was suppressed after Ala-Gln treatment, the effect of which might be dependent on the elevation of SOD and GPX activities, and on GSH levels in liver. Interestingly, we observed that Ala-Gln clearly inhibited LPS/D-Gal exposure-induced macrophage accumulation and the production of proinflammatory factors in the liver. Furthermore, Ala-Gln greatly regulated autophagy in the liver in LPS/D-Gal-treated mice. Using RAW264.7 cells, we confirmed the anti-inflammatory role of Ala-Gln-targeting macrophages.

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“…Furthermore, Oliveira and cols. Demonstrated an important reduction on TNF-α, NF-κB, IL-6, and HO-1, inflammatory mediators in pretreated gerbils with L-Ala-Gln [42].…”

Section: Use Of Omega 3 6 and 9 In Brain Ischemia Animal Modelsmentioning

confidence: 94%

The Pathophysiological Aspects of Cerebral Diseases

Silva¹,

Maia²,

Vasconcelos³

et al. 2022

Cerebrovascular Diseases - Elucidating Key Principles

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Introduction. Cerebrovascular disorders are the main causes of heavy burden health worldwide, also, it is critical to understand the pathophysiological mechanism and then trying to prevent the neurological sequels. Objective. To discuss the inflammatory and oxidative stress aspects associated to the cerebrovascular diseases, focusing on biomarkers, also the role of omega oils, and the intracellular molecular network associated to the tissue burden on those conditions. Results. One of the most promising biomarkers it is Neuron-Specific Enolase (NSE). Serum NSE levels were elevated in stroke-patients compared to the non-stroke controls. Also, studies have demonstrated that in specific ratio omega oils 3, 6 and 9 can ameliorate the inflammatory and oxidative stress in nervous tissue and could be useful to the inflammatory and oxidative stress negative effects of cerebrovascular diseases. In addition, the study of the molecular mechanisms is essential to understand which molecules could be addressed in cascade of events preventing the permanent damage on the nervous tissue. Final considerations. The studies on cerebrovascular disorders must precisely identify the mechanisms and key molecules involved and improve the time of diagnostics and prognostics reducing the negative impacts of those conditions.

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Preconditioning with L-Ala-Gln reduces the expression of inflammatory markers (TNF-α, NF-κB, IL-6 and HO-1) in an injury animal model of cerebrovascular ischemia in Meriones unguiculatus (gerbils)

Cited by 8 publications

References 26 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

Alanyl-Glutamine Protects against Lipopolysaccharide-Induced Liver Injury in Mice via Alleviating Oxidative Stress, Inhibiting Inflammation, and Regulating Autophagy

The Pathophysiological Aspects of Cerebral Diseases

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