Impact of intracellular glyceraldehyde-derived advanced glycation end-products on human hepatocyte cell death.
作者： Akiko Sakasai-Sakai , Takanobu Takata , Jun-ichi Takino , Masayoshi Takeuchi
DOI: 10.1038/S41598-017-14711-3
关键词: Programmed cell death 、 Necrosis 、 Cancer research 、 DNA damage 、 Glycation 、 Camptothecin 、 Hepatocyte 、 Apoptosis 、 Intracellular 、 Chemistry
摘要: Hepatocyte cell death is a key feature of nonalcoholic steatohepatitis (NASH); however, the pathogenesis NASH currently remains unclear. We aimed to investigate effects intracellular glyceraldehyde (GA)-derived advanced glycation end-products (GA-AGEs) on human hepatocyte death. The accumulation GA-AGEs has been associated with induction DNA damage and necrotic Among GA-AGEs, caspase-3 identified as GA-AGE-modified protein abrogated function. Furthermore, activation apoptosis by camptothecin, DNA-damaging agent, was suppressed treatment GA. These results suggest inhibitory DNA-damage-induced apoptosis, which necrosis. Therefore, suppression necrosis, inflammatory form death, may represent novel therapeutic target for NASH.
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