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Provedor de dados: |
BJMBR
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País: |
Brazil
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Título: |
Adiponectin is protective against endoplasmic reticulum stress-induced apoptosis of endothelial cells in sepsis
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Autores: |
Hou,Yun
Wang,Xi Feng
Lang,Zhi Qiang
Jin,Yin Chuan
Fu,Jia Rong
Xv,Xiao Min
Sun,Shi Tian
Xin,Xin
Zhang,Lian Shuang
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Data: |
2018-01-01
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Ano: |
2018
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Palavras-chave: |
Adiponectin
Apoptosis
Endoplasmic reticulum stress
Endothelial cell
Sepsis
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Resumo: |
Endoplasmic reticulum (ER) stress is a critical molecular mechanism involved in the pathogenesis of sepsis. Hence, strategies for alleviating this stress may be essential for preventing cardiovascular injuries under sepsis. Adiponectin is secreted by adipocytes and its levels are decreased in sepsis. The purpose of this study was to investigate the protective effects of adiponectin treatment on endothelial cells and its mechanism. Male Wistar rats underwent cecal ligation and puncture (CLP) before being treated with adiponectin (72 and 120 μg/kg). The levels of malondialdehyde (MDA) in plasma, histological structure, and apoptosis of endothelial cells were evaluated. In vitro, human umbilical vein endothelial cells (HUVECs) were treated with adiponectin at 10 and 20 μg/mL for 24 h after stimulation by lipopolysaccharide (LPS). The levels of reactive oxygen species (ROS), ultrastructure, rate of apoptosis, the expression of inositol-requiring enzyme 1α (IRE1α) protein, and its downstream molecules (78 kDa glucose-regulated protein (GRP78), C/EBP homologous protein (CHOP), and caspase-12) were detected. The results showed that the levels of MDA and ROS induced by CLP or LPS stimulation were increased. Furthermore, endothelial cell apoptosis was increased under sepsis. The IRE1α pathway was initiated, as evidenced by activated IRE1α, increased GRP78, and up-regulated CHOP and caspase-12 in HUVECs. Following treatment with adiponectin, the number of apoptotic endothelial cells was markedly decreased. These findings demonstrated that treatment with adiponectin decreased apoptosis of endothelial cells caused by sepsis by attenuating the ER stress IRE1α pathway activated by oxidative stress.
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Tipo: |
Info:eu-repo/semantics/article
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Idioma: |
Inglês
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Identificador: |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2018001200609
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Editor: |
Associação Brasileira de Divulgação Científica
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Relação: |
10.1590/1414-431x20187747
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Formato: |
text/html
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Fonte: |
Brazilian Journal of Medical and Biological Research v.51 n.12 2018
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Direitos: |
info:eu-repo/semantics/openAccess
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