The downregulation of thioredoxin accelerated Neuro2a cell apoptosis induced by advanced glycation end product via activating several pathways
作者： Xiang Ren , Haiying Ma , Yuanyuan Qiu , Bo Liu , Hui Qi
DOI: 10.1016/J.NEUINT.2015.06.009
关键词:
摘要: Abstract Thioredoxin (Trx), a 12 kDa protein, has different functions in cellular environments, playing important anti-oxidative and anti-apoptotic roles regulating the expression of transcription factors. Advanced glycation end products (AGEs) are heterogeneous group irreversible adducts from glucose–protein condensation reactions considered crucial to development diabetic nephropathy, retinopathy, neurodegeneration atherosclerosis. The aim this study was use Trx inhibitor investigate effects mechanism down-regulation on AGE-induced Neuro2a cell apoptosis. cells were cultured vitro treated with conditions. apoptosis proliferation detected using flow cytometry, DNA-Ladder CCK8 assays. Rho 123 used detect mitochondrial membrane potential. ROS generation caspase3 activity DCFH-DA probe micro-plate reader. Western blotting real-time PCR proteins genes. We found that thioredoxin could accelerate cells. A possible underlying is stimulated up-regulation ASK1, p-JNK, PTEN, Txnip, as well p-AKT, ultimately increasing levels activity.
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