Theaflavin alleviates inflammatory response and brain injury induced by cerebral hemorrhage via inhibiting the nuclear transcription factor kappa β-related pathway in rats

The cytotoxicity of docosahexaenoic acid (DHA) on normal cells is still unclear. This study investigated the effects of DHA on the cytotoxicity and possible mechanism in the BRL-3A cell. The cultured rat liver BRL-3A cell line was treated with 50, 100 and 200 μM DHA for 24 h. The cell viability was increased in the 50 and 100 μM DHA treatments, but decreased in the 200 μM DHA treatment. The 50, 100 and 200 μM DHA treatments increased the proportion of the apoptotic cells, the levels of lactate dehydrogenase (LDH), alkaline phosphatase (AKP) and IL-6 in the supernatant, and the ratio of the phosphonated p38MAPK to the p38MAPK (p-p38/p38) protein in the cells. The expression of TGF beta-activated kinase 1 (TAK1), nuclear transcription factor-κB p65 (NF-κB p65) and the inhibitor of NF-κB alpha (IκBα) mRNA, and the ratio of the phosphonated IκBα (p-IκBα) to IκBα protein were increased in the 200 μM DHA treatment, while the ratio of phosphonated extracellular regulated protein kinases (p-ERK) to ERK protein was decreased in the 200 μM DHA treatment. These results indicate that DHA-treated (50, 100 and 200 μM) BRL-3A cells for 24 h promotes cell apoptosis and inflammatory response, and the p38 MAPK, ERK and NF-κB signal pathways were involved in mediating the apoptosis and inflammatory response.

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ROLE OF TRANSCRIPTIONAL FACTOR NF-κB IN DEVELOPMENT OF OXIDATIVE STRESS IN HEART OF RATS DURING SYSTEMIC INFLAMMATORY RESPONSE INDUCED BY BACTERIAL LIPOPOLYSACCHARIDE

Актуальні проблеми сучасної медицини Вісник Української медичної стоматологічної академії ◽

10.31718/2077-1096.19.3.108 ◽

2019 ◽

Vol 19 (3) ◽

pp. 108-112

Author(s):

O.Ye. Akimov ◽

A.Yu. Vetkina ◽

A.I. Malyk ◽

A.D. Shkodina ◽

S.V. Denysenko ◽

...

Keyword(s):

Oxidative Stress ◽

Transcription Factor ◽

Inflammatory Response ◽

Catalase Activity ◽

No Synthase ◽

Systemic Inflammatory Response ◽

Bacterial Lipopolysaccharide ◽

Male Rats ◽

Nuclear Transcription Factor ◽

Basic Production

Systemic inflammatory response syndrome (SIRS) is a threatening complication that can lead to myocardial infarction. Activation of the nuclear transcription factor κB (NF-κB) plays an unambiguous role in the SIRS development. The purpose of this study is to determine the effect of NF-κB nuclear transcription factor activation on production of superoxide anion radical (O2•-), superoxide dismutase (SOD) and catalase activity, concentration of free malondialdehyde (MDA) in the heart of rats during SIRS modelling. The experiment was performed on 24 mature Wistar male rats weighing 180-220 g. Animals were divided into 3 groups consisting of 8 animals (control, SIRS group, NF-κB blockade group). SIRS was modelled by intraperitoneal administration of bacterial lipopolysaccharide (Pyrogenal) in a dose of 0.4 μg / kg 3 times a week in the first week; then once a week for 2 months. The blockade of NF-κB was performed by administration of ammonium pyrrolidine dithiocarbamate (PDTC) in a dose of 76 mg / kg. Production of O2•-, activities of SOD and catalase, concentration of MDA was investigated in 10% heart tissues homogenate. Induction of SIRS by Pyrogenal increases basic production of O2•- by 54.6% compared to the control group. Production of O2•- by microsomal electron transport chain (ETC) and NO synthase increases by 52.9%; production of O2•- by mitochondrial ETC increases by 38,9%. Activity of SOD increases by 1.86 times, activity of catalase increases by 1.53 times. The concentration of free MDA in heart tissues has grown by 81.2%. Blockade of the transcription factor NF-κB reduces basic production of O2•- by 38.9%; by microsomal ETC and NO synthase by 41%; by mitochondrial ETC by 22.2% compared to SIRS group. SOD activity decreases by 56.7%, while catalase activity does not statistically significantly change. The concentration of free MDA in heart tissues decreases by 31.4%. Activation of the nuclear transcription factor NF-κB in the heart of rats during SIRS induced by Pyrogenal leads to an increase in O2•- production with subsequent development of oxidative stress. Compensatory activation of antioxidant enzymes under these conditions is not able to prevent the development of oxidative stress in heart tissues.

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Shiga taxin type 2 but not type 1 induces interleukin-12 expression from peripheral blood mononuclear cells via activated nuclear transcription factor-kB

Gastroenterology ◽

10.1016/s0016-5085(01)81612-7 ◽

2001 ◽

Vol 120 (5) ◽

pp. A324-A324

Author(s):

M TATEWAKI ◽

H NAKAO ◽

H NOGAMI ◽

E HOSHINO ◽

H MOTEGI ◽

...

Keyword(s):

Transcription Factor ◽

Peripheral Blood Mononuclear Cells ◽

Peripheral Blood ◽

Mononuclear Cells ◽

Interleukin 12 ◽

Peripheral Blood Mononuclear ◽

Nuclear Transcription Factor ◽

Blood Mononuclear Cells

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Roles of osteopontin and nuclear transcription factor in chronic cyclosporine nephrotoxicity

Academic Journal of Second Military Medical University ◽

10.3724/sp.j.1008.2014.00476 ◽

2014 ◽

Vol 35 (5) ◽

pp. 476

Author(s):

Mei-rong FANG ◽

Ying-shun JIN ◽

Ji-zhe JIN ◽

Zhen-hua CUI ◽

Hai-feng JIN ◽

...

Keyword(s):

Transcription Factor ◽

Nuclear Transcription Factor ◽

Cyclosporine Nephrotoxicity

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LncRNA Blnc1 mediates the permeability and inflammatory response of cerebral hemorrhage by regulating the PPAR-γ/SIRT6/FoxO3 pathway

Life Sciences ◽

10.1016/j.lfs.2020.118942 ◽

2021 ◽

Vol 267 ◽

pp. 118942

Author(s):

Lijuan Xie ◽

Yingying Wang ◽

Zhuo Chen

Keyword(s):

Inflammatory Response ◽

Cerebral Hemorrhage ◽

Ppar Γ

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Localized pancreatic NF-κB activation and inflammatory response in taurocholate-induced pancreatitis

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.2001.280.6.g1197 ◽

2001 ◽

Vol 280 (6) ◽

pp. G1197-G1208 ◽

Cited By ~ 104

Author(s):

Eva Vaquero ◽

Ilya Gukovsky ◽

Vjekoslav Zaninovic ◽

Anna S. Gukovskaya ◽

Stephen J. Pandol

Keyword(s):

Transcription Factor ◽

Inflammatory Response ◽

Pancreatic Head ◽

Pancreatic Injury ◽

Nuclear Factor Κb ◽

Saline Infusion ◽

Activator Protein 1 ◽

Local Inflammatory Response ◽

Monocyte Chemoattractant Protein 1 ◽

Factor Α

Transcription factor nuclear factor-κB (NF-κB) is activated in cerulein pancreatitis and mediates cytokine expression. The role of transcription factor activation in other models of pancreatitis has not been established. Here we report upregulation of NF-κB and inflammatory molecules, and their correlation with local pancreatic injury, in a model of severe pancreatitis. Rats received intraductal infusion of taurocholate or saline, and the pancreatic head and tail were analyzed separately. NF-κB and activator protein-1 (AP-1) activation were assessed by gel shift assay, and mRNA expression of interleukin-6, tumor necrosis factor-α, KC, monocyte chemoattractant protein-1, and inducible nitric oxide synthase was assessed by semiquantitative RT-PCR. Morphological damage and trypsin activation were much greater in the pancreatic head than tail, in parallel with a stronger activation of NF-κB and cytokine mRNA. Saline infusion mildly affected these parameters. AP-1 was strongly activated in both pancreatic segments after either taurocholate or saline infusion. NF-κB inhibition with N-acetylcysteine ameliorated the local inflammatory response. Correlation between localized NF-κB activation, cytokine upregulation, and tissue damage suggests a key role for NF-κB in the development of the inflammatory response of acute pancreatitis.

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Angiotensin II activates nuclear transcription factor-κB through AT1 and AT2 receptors11See Editorial by Luft, p. 2272.

Kidney International ◽

10.1046/j.1523-1755.2002.00365.x ◽

2002 ◽

Vol 61 (6) ◽

pp. 1986-1995 ◽

Cited By ~ 145

Author(s):

Gunter Wolf ◽

Ulrich Wenzel ◽

Kevin D. Burns ◽

Raymond C. Harris ◽

Rolf A.K. Stahl ◽

...

Keyword(s):

Transcription Factor ◽

Angiotensin Ii ◽

Nuclear Transcription Factor

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Influence of Glutamine on Intestinal Inflammatory Response, Mucosa Structure Alterations and Apoptosis following Traumatic Brain Injury in Rats

Journal of International Medical Research ◽

10.1177/147323000703500509 ◽

2007 ◽

Vol 35 (5) ◽

pp. 644-656 ◽

Cited By ~ 12

Author(s):

D Feng ◽

W Xu ◽

G Chen ◽

C Hang ◽

H Gao ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Inflammatory Response ◽

Intestinal Inflammation ◽

Glutamine Supplementation ◽

Intercellular Adhesion Molecule ◽

Intercellular Adhesion Molecule 1 ◽

Tissue Samples ◽

Weight Drop ◽

Factor Α

Traumatic brain injury (TBI) can induce a persistent inflammatory response, histopathological changes and apoptosis in the intestine. Glutamine has been shown to reduce bacterial translocation and maintain intestine mucosal integrity, but its effects on the inflammatory response, structural alterations and apoptosis in intestinal mucosa following TBI have not been previously investigated. Using the weight-drop method, a right parietal cortical contusion was induced in rats and, for the next 5 days, they were fed either chow alone or chow mixed with glutamine. Intestinal tissue samples were then removed for analysis. Following TBI, glutamine supplementation was found to: decrease intestinal concentrations of interleukin (IL) −1β, tumour necrosis factor-α (TNF-α) and IL-6; downregulate intercellular adhesion molecule-1 (ICAM-1) expression; attenuate TBI-induced damage to the intestine structure; and reduce apoptosis. These results suggest that post-TBI glutamine administration could suppress intestinal inflammation, protect intestinal mucosal structure and reduce mucosal apoptosis.

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