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Geniposide prevents rotenone-induced apoptosis in primary cultured neurons
Author(s) -
Lin Li,
Juan Zhao,
Ke Liu,
Guanglai Li,
Yanqing Han,
Yueze Liu
Publication year - 2015
Publication title -
neural regeneration research/neural regeneration research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.93
H-Index - 38
eISSN - 1876-7958
pISSN - 1673-5374
DOI - 10.4103/1673-5374.167760
Subject(s) - rotenone , neuroprotection , apoptosis , pharmacology , agonist , lactate dehydrogenase , chemistry , western blot , receptor , caspase 3 , microbiology and biotechnology , programmed cell death , biology , biochemistry , mitochondrion , enzyme , gene
Geniposide, a monomer extracted from gardenia and widely used in Chinese medicine, is a novel agonist at the glucagon-like peptide-1 receptor. This receptor is involved in neuroprotection. In the present study, we sought to identify an anti-apoptotic mechanism for the treatment of neurodegenerative diseases. Primary cultured neurons were treated with different concentrations of rotenone for 48 hours. Morphological observation, cell counting kit-8 assay, lactate dehydrogenase detection and western blot assay demonstrated that 0.5 nM rotenone increased lactate dehydrogenase release, decreased the expression of procaspase-3 and Bcl-2, and increased cleaved caspase-3 expression in normal neurons. All these effects were prevented by geniposide. Our results indicate that geniposide diminished rotenone-induced injury in primary neurons by suppressing apoptosis. This may be one of the molecular mechanisms underlying the efficacy of geniposide in the treatment of neurodegenerative diseases.

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