scholarly journals Toxic Effects of Docosahexaenoic Acid Treatment in the Rat Liver BRL-3A Cell

Toxics ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 112
Author(s):  
Wenli Luo ◽  
Li Li ◽  
Weina Xu ◽  
Jing Zhang ◽  
Jianxiong Xu

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.

2004 ◽  
Vol 18 (6) ◽  
pp. 749-750 ◽  
Author(s):  
Zsolt Radák ◽  
Hae Young Chung ◽  
Hisashi Naito ◽  
Ryoya Takahashi ◽  
Kyung Jin Jung ◽  
...  

Author(s):  
O.Ye. Akimov ◽  
A.Yu. Vetkina ◽  
A.I. Malyk ◽  
A.D. Shkodina ◽  
S.V. Denysenko ◽  
...  

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.


2014 ◽  
Vol 35 (5) ◽  
pp. 476
Author(s):  
Mei-rong FANG ◽  
Ying-shun JIN ◽  
Ji-zhe JIN ◽  
Zhen-hua CUI ◽  
Hai-feng JIN ◽  
...  

1984 ◽  
Vol 259 (9) ◽  
pp. 5776-5783 ◽  
Author(s):  
M VanRollins ◽  
R C Baker ◽  
H W Sprecher ◽  
R C Murphy

2001 ◽  
Vol 280 (6) ◽  
pp. G1197-G1208 ◽  
Author(s):  
Eva Vaquero ◽  
Ilya Gukovsky ◽  
Vjekoslav Zaninovic ◽  
Anna S. Gukovskaya ◽  
Stephen J. Pandol

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.


AGE ◽  
2012 ◽  
Vol 35 (3) ◽  
pp. 597-608 ◽  
Author(s):  
Fei Gao ◽  
Ameer Y. Taha ◽  
Kaizong Ma ◽  
Lisa Chang ◽  
Dale Kiesewetter ◽  
...  

1997 ◽  
Vol 267 (3) ◽  
pp. 673-683 ◽  
Author(s):  
Oliver Schott ◽  
Martin Billeter ◽  
Barbara Leiting ◽  
Gerhard Wider ◽  
Kurt Wüthrich

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