4.5 Article

Dimethyl Fumarate Modulates Oxidative Stress and Inflammation in Organs After Sepsis in Rats

期刊

INFLAMMATION
卷 41, 期 1, 页码 315-327

出版社

SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-017-0689-z

关键词

sepsis; oxidative stress; inflammation; organ injury

资金

  1. CNPq
  2. CAPES

向作者/读者索取更多资源

Sepsis is defined as life-threatening organ dysfunction induced by a disrupted host response to infecting pathogens. Evidences suggest that oxidative stress is intrinsically related to sepsis progression. Dimethyl fumarate (DMF) is a novel oral therapeutic agent with anti-oxidant properties which exerts protective effects through activation of nuclear factor erythroid 2 (NFE2)-related factor 2 (Nrf2). Thus, the aim of this study is to evaluate the effect of DMF in different organs of rats submitted to an animal model of sepsis. Adult male Wistar rats were subjected to sepsis by cecal ligation and puncture (CLP) procedure and sham-operated rats was considered control group. The experimental groups were divided into sham + vehicle, sham + DMF, sham + NAC, CLP + vehicle, CLP + DMF, and CLP + NAC. Rats were treated by oral gavage with DMF immediately after and 12 h after surgery, or NAC (s.c.) at 3, 6, and 12 h after surgery. Twenty-four hours after sepsis induction, neutrophil infiltration, nitrite/nitrate concentrations, oxidative damage to lipids and proteins, superoxide dismutase (SOD), and catalase (CAT) activities were evaluated in the heart, liver, lung, and kidney. Septic animals presented increased neutrophil infiltration, NO metabolism, oxidative damage to lipids and proteins, and decreases of SOD and CAT activities, mainly in the heart, liver, and lung, while DMF-treated animals showed significant reduction in neutrophil infiltration, NO metabolism, and oxidative damage followed by increased SOD and CAT activities. DMF is effective in preventing oxidative stress and inflammation in rats 24 h after sepsis induction.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.5
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

Article Neurosciences

Stanniocalcin 1 Inhibits the Inflammatory Response in Microglia and Protects Against Sepsis-Associated Encephalopathy

Sandra Bonfante, Larissa Joaquim, Maria Eduarda Fileti, Amanda Della Giustina, Mariana Pereira de Souza Goldim, Lucineia Gainski Danielski, Evandro Cittadin, Raquel Jaconi De Carli, Bianca Xavier de Farias, Nicole Alessandra Engel, Naiana Rosa, Jucelia Jeremias Fortunato, Vijayasree Giridharan, Giselli Scaini, Gislaine Tezza Rezin, Jaqueline Generoso, Rafael Mariano de Bitencourt, Silvia Terra, Tatiana Barichello, Fabricia Petronilho

Summary: STC-1 has been shown to have a protective role by inhibiting the inflammatory response, reducing oxidative stress, and improving mitochondrial function, thereby providing neuroprotection against sepsis-associated encephalopathy.

NEUROTOXICITY RESEARCH (2021)

Article Biochemistry & Molecular Biology

Requirement of brain interleukin33 for aquaporin4 expression in astrocytes and glymphatic drainage of abnormal tau

Jean Wu, Colin Carlock, Junbo Shim, Ines Moreno-Gonzalez, William Glass, April Ross, Tatiana Barichello, Joao Quevedo, Yahuan Lou

Summary: IL33 is essential for regulating the expression of AQP4 in astrocytes, with its deficiency leading to abnormal tau accumulation in neurons and impaired drainage. This study suggests that different forms of AQP4 play distinct roles in glymphatic drainage, with p-AQP4 driving flow toward perivenous space while n-AQP4 may help remove neuronal wastes. Defects in IL33-related mechanisms may contribute to chronic neurodegeneration and tauopathy in aging mice.

MOLECULAR PSYCHIATRY (2021)

Article Neurosciences

NLRP3 inflammasome activation increases brain oxidative stress after transient global cerebral ischemia in rats

Larissa Silva Joaquim, Lucineia Gainski Danielski, Sandra Bonfante, Erica Biehl, Khiany Mathias, Tais Denicol, Erick Bagio, Everton Venicius Lanzzarin, Richard Simon Machado, Gabriela Costa Bernades, Jaqueline Generoso, Amanda Della Giustina, Tatiana Barichello, Fabricia Petronilho

Summary: The study demonstrates that inhibiting NLRP3 activation with MCC950 can reduce brain oxidative damage after cerebral ischemia/reperfusion in rats.

INTERNATIONAL JOURNAL OF NEUROSCIENCE (2023)

Article Neurosciences

Combination of electroconvulsive stimulation with ketamine or escitalopram protects the brain against inflammation and oxidative stress induced by maternal deprivation and is critical for associated behaviors in male and female rats

Helena M. Abelaira, Thayse Rosa, Airam B. de Moura, Natalia M. Andrade, Nicoly S. Martinello, Larissa R. Maciel, Maria Eduarda M. Botelho, Laura A. Borba, Beatriz C. Chede, Camila O. Arent, Larissa Joaquim, Sandra Bonfante, Lucineia G. Danielski, Talita Tuon, Fabricia Petronilho, Joao Quevedo, Gislaine Z. Reus

Summary: This study evaluated the treatment effects of ketamine, electroconvulsive stimulation (ECS), escitalopram, alone or in combination, in adult male and female rats subjected to maternal deprivation (MD) animal model. The findings showed that the treatments were able to reverse depressive and anhedonic behavior in females, while elicited different responses in males. Furthermore, the study highlights the importance of considering gender differences in MDD related to early stress and therapeutic strategies.

MOLECULAR NEUROBIOLOGY (2022)

Editorial Material Psychiatry

What is the role of microbial infection in Alzheimer's disease?

Tatiana Barichello, Vijayasree V. Giridharan, Clarissa M. Comim, Rodrigo Morales

BRAZILIAN JOURNAL OF PSYCHIATRY (2022)

Article Immunology

A crosstalk between gut and brain in sepsis-induced cognitive decline

Vijayasree V. Giridharan, Jaqueline S. Generoso, Leonardo Lence, Gabriela Candiotto, Emilio Streck, Fabricia Petronilho, Anilkumar Pillai, Tarek Sharshar, Felipe Dal-Pizzol, Tatiana Barichello

Summary: Sepsis disrupts the microbiota-gut-brain axis homeostasis and leads to cognitive impairment. Survivors of sepsis show significant decline in memory and learning. Understanding the function of glial cells and gut microbiota can provide new approaches for treating sepsis patients.

JOURNAL OF NEUROINFLAMMATION (2022)

Article Neurosciences

Lung-Brain Crosstalk in Sepsis: Protective Effect of Prophylactic Physical Exercise Against Inflammation and Oxidative Stress in Rats

Amanda Della Giustina, Judite Filgueiras Rodrigues, Erick Bagio, Sandra Bonfante, Larissa Joaquim, Graciela Zarbato, Solange Stork, Richard Simon Machado, Mariana Pereira de Souza Goldim, Lucineia Gainski Danielski, Khiany Mathias, Carlos Dacoregio, Taise Cardoso, Giulia S. Predroso, Ligia Milanez Venturini, Rubya Pereira Zaccaron, Paulo Cesar Lock Silveira, Ricardo Aurino Pinho, Fabricia Petronilho

Summary: Sepsis is a life-threatening condition caused by a dysregulated response to infection, which leads to organ dysfunction. Inflammation and oxidative stress play major roles in the damage to the lungs and brain in sepsis. A physical exercise program has protective effects against inflammation and oxidative stress in the lungs and brain of septic rats.

MOLECULAR NEUROBIOLOGY (2022)

Article Neurosciences

The Many Faces of Astrocytes in the Septic Brain

Lucineia Gainski Danielski, Amanda Della Giustina, Fernanda Frederico Gava, Tatiana Barichello, Fabricia Petronilho

Summary: Sepsis is a life-threatening condition that can lead to cognitive and memory damage, which may be associated with astrocytic activation and the release of inflammatory mediators.

MOLECULAR NEUROBIOLOGY (2022)

Review Endocrinology & Metabolism

The Infected Lungs and Brain Interface in COVID-19: The Impact on Cognitive Function

Larissa Joaquim, Amanda Della Giustina, Richard Simon Machado, Kiuanne Lino Lobo Metzker, Sandra Bonfante, Lucineia Gainski Danielski, Mariana Pereira de Souza Goldim, Fabricia Petronilho

Summary: Recovered COVID-19 patients may experience neurological, psychiatric, and cognitive problems, although the exact prevalence and outcome of cognitive sequelae are unclear. The mechanisms behind COVID-19-induced cognitive dysfunction may involve neuroinflammation mediated by sustained systemic inflammation, disrupted brain barrier, and glial reactiveness.

NEUROIMMUNOMODULATION (2022)

Article Biochemistry & Molecular Biology

Sepsis exacerbates Alzheimer's disease pathophysiology, modulates the gut microbiome, increases neuroinflammation and amyloid burden

Vijayasree V. Giridharan, Celso S. G. Catumbela, Carlos Henrique R. Catalao, Juneyoung Lee, Bhanu P. Ganesh, Fabricia Petronilho, Felipe Dal-Pizzol, Rodrigo Morales, Tatiana Barichello

Summary: In this study, it was found that peripheral infection may be a risk factor for Alzheimer's disease pathology, and infection can accelerate cognitive decline and AD pathology. By inducing a polymicrobial infection in APP/PS1 mice through cecal ligation and puncture surgery, the study showed that sepsis led to increased Aβ deposition and activation of microglia around Aβ plaques in the brain. Furthermore, sepsis affected gut microbiome composition and structure, as well as short-chain fatty acid levels.

MOLECULAR PSYCHIATRY (2023)

Review Critical Care Medicine

Biomarkers for sepsis: more than just fever and leukocytosis-a narrative review

Tatiana Barichello, Jaqueline S. Generoso, Mervyn Singer, Felipe Dal-Pizzol

Summary: A biomarker is a measurable indicator of a patient's clinical condition that can be measured accurately and reproducibly. In sepsis patients, there are various biomarkers such as PRMs, complement system, and cytokines. However, further research is needed to identify the optimal combinations of biomarkers.

CRITICAL CARE (2022)

暂无数据