scholarly journals Gastrodin Ameliorates Cognitive Dysfunction in Diabetes Rat Model via the Suppression of Endoplasmic Reticulum Stress and NLRP3 Inflammasome Activation

2018 ◽  
Vol 9 ◽  
Author(s):  
Tianyuan Ye ◽  
Xiangbao Meng ◽  
Yadong Zhai ◽  
Weijie Xie ◽  
Ruiying Wang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cognitive Dysfunction ◽  
Rat Model ◽  
Nlrp3 Inflammasome ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation

scholarly journals Burn Plus Lipopolysaccharide Augments Endoplasmic Reticulum Stress and NLRP3 Inflammasome Activation and Reduces PGC-1α in Liver

Shock ◽  
2014 ◽  
Vol 41 (2) ◽  
pp. 138-144 ◽  
Author(s):  
Li Diao ◽  
Alexandra H. Marshall ◽  
Xiaojing Dai ◽  
Elena Bogdanovic ◽  
Abdikarim Abdullahi ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Nlrp3 Inflammasome ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation

scholarly journals H3 relaxin alleviated vascular injury  in rats with type 1 diabetes by inhibiting endoplasmic reticulum stress and inflammation

2021 ◽  
Author(s):  
Xiaohui Zhang ◽  
Kelaier Yang ◽  
Jinyu Chi ◽  
Wenjia Chen ◽  
Xiao Ma ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Type 1 Diabetes ◽  
Endoplasmic Reticulum Stress ◽  
Nlrp3 Inflammasome ◽  
Vascular Function ◽  
Diabetic Rats ◽  
Inflammasome Activation ◽  
Type I ◽  
Nlrp3 Inflammasome Activation

Abstract Human recombinant relaxin-3 (H3 relaxin ),a small molecule peptide hormone, ameliorated myocardial injury after myocardial infarction or isoprenaline injection by inhibiting apoptosis and fibrosis. However, whether H3 relaxin protects vascular function in rats with type 1 diabetes and its mechanism are unknown. In type 1 diabetes rats model induced by streptozotocin (STZ), rats were subcutaneously injected H3 relaxin (2 µg/kg/d or 0.2 µg/kg/d) for 2 weeks. At 4 or 8 weeks after STZ injection, we detected the expression of fibrosis (type I and III collagen), ERS (endoplasmic reticulum stress) and NLRP3 inflammasome activation in the aortas and inflammation markers in the plasma from rats with diabetes. Compared with the diabetic rats, H3 relaxin treatment exhibited markedly decreased plasma oxidative stress markers (TNF-a and MDA) levels. The protein expression levels of type I and III collagen in the aortas were increased in rats with diabetes, inhibited by H3 relaxin. H3 relaxin treatment inhibited ERS (GRP78 and CHOP) and NLRP3 inflammasome activation in the aortas of diabetic rats. These results suggest that H3 relaxin inhibited fibrosis, ERS and inflammation activation in the aortas of type 1 diabetic rats.

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