Abstract:
:Alzheimer's disease is an age-related neurodegenerative disease, associated with the presence of extracellular amyloid-β (Aβ) plaques and neurofibrillary tangles. Although the pathogenesis of AD remains unclear, the characteristic feature of AD was reported to be the buildup of Aβ plaques. In this study, we extensively investigated the neuroprotective effects of 2-substituted 1,3-selenazole amide derivatives (CHF11) on Aβ1-42 transgenic Caenorhabditis elegans CL4176. Results showed that worms fed with CHF11 exhibited remarkably reduced paralysis, decreased levels of toxic Aβ oligomers and Aβ plaque deposition, as well as less ROS production in comparison with the untreated worms. The effective concentrations of CHF11 were arranged in the descending order of 100 µM > 10 µM > 1 µM. Real-time PCR analysis showed that there was no significant difference in Aβ expression between CHF11-administered group and the blank control group, suggesting that CHF11-induced reduction in toxic protein deposition may be regulated at the post-transcriptional level. In the meantime, the gene expressions of hsf-1 and its downstream target hsp-12.6 were significantly increased, indicating that CHF11 against Aβ toxicity may involve in HSF-1 signaling pathway in worms. In conclusion, CHF11 exhibits a significant protective effect against β-amyloid-induced toxicity in CL4176 by reducing β-amyloid aggregation and ROS production, which may involve in HSF-1 and downstream target HSP-12.6 pathway.
journal_name
Neurotox Resjournal_title
Neurotoxicity researchauthors
Wang H,Yue Y,Zhao H,Wu H,Jiang K,Li S,Zhao M,Lin Fdoi
10.1007/s12640-020-00321-xsubject
Has Abstractpub_date
2021-01-05 00:00:00eissn
1029-8428issn
1476-3524pii
10.1007/s12640-020-00321-xpub_type
杂志文章abstract::Microglial activation and subsequent release of toxic pro-inflammatory factors are believed to play an important role in neuronal cell death associated with Parkinson's disease (PD). Compounds that inhibit microglia activation and suppress pro-inflammatory factor release have been reported to have neuroprotective effe...
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journal_title:Neurotoxicity research
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journal_title:Neurotoxicity research
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journal_title:Neurotoxicity research
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journal_title:Neurotoxicity research
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doi:10.1007/s12640-016-9603-y
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journal_title:Neurotoxicity research
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journal_title:Neurotoxicity research
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journal_title:Neurotoxicity research
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journal_title:Neurotoxicity research
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