Abstract
BackgroundMitochondrial dysfunction has been implicated in neuronal apoptosis associated with neurodegenerative diseases such as Huntington’s disease (HD). Animals that are administered 3-nitropropionic acid (3-NP), a mitochondrial toxin that specifically inhibits complex II of the mitochondrial electron transport chain, manifest HD-like symptoms.MethodsPsoralea corylifolia Linn seed extracts against 3-NP induced mitochondrial dysfunction in cultured rat pheochromocytoma (PC12) cells, which are used for neurobiological studies.ResultsIn this study showed that 3-NP-treated PC12 cells had decreased ATP levels, lower cellular oxygen consumption, and reduced mitochondrial membrane potential than those of untreated PC12 cells. Psoralea corylifolia Linn seed extracts stimulated mitochondrial respiration with uncoupling and induced an increased bioenergetic reserve capacity. Furthermore, PC12 cells pretreated with P. corylifolia Linn seed extracts significantly attenuated 3-NP-induced cell death, reduced ATP levels, and lowered the mitochondrial membrane potential.ConclusionsThese results demonstrate that P. corylifolia Linn seed extracts have a significant protective effect against 3-NP induced cytotoxicity. Thus, our results indicate that P. corylifolia Linn seed extracts may have potential applications as therapeutic agents for treating neurodegenerative disease.
Highlights
Mitochondrial dysfunction has been implicated in neuronal apoptosis associated with neurodegenerative diseases such as Huntington’s disease (HD)
We investigated the neuroprotective effect of P. corylifolia seed extracts against 3-nitropropionic acid (3-NP) induced mitochondrial dysfunction in cultured rat pheochromocytoma (PC12) cells, which are widely used for neurobiological studies
Pretreatment with PCWE for 24 h followed by 3-NP exposure resulted in higher viability than that of 3-NP exposed PC12 cells that were not pretreated with PCWE
Summary
Mitochondrial dysfunction has been implicated in neuronal apoptosis associated with neurodegenerative diseases such as Huntington’s disease (HD). Animals that are administered 3-nitropropionic acid (3-NP), a mitochondrial toxin that inhibits complex II of the mitochondrial electron transport chain, manifest HD-like symptoms. 3-nitropropionic acid (3-NP) is a specific inhibitor of mitochondrial respiratory complex II and can cause HD -like symptoms in animals upon ingestion [10]. A previous study showed that complex II inhibition by 3-NP resulted in mitochondrial fragmentation and neuronal cell death via N-methyl-D-aspartate and reactive oxygen species (ROS)-dependent pathways [11]. Mitochondrial electron leakage causes oxidative stress that can lead to cell death. The mechanisms underlying oxidative damageinduced neuronal death are poorly understood, and whether mitochondrial defects are the primary cause of toxicity or a secondary response to the damage remains unknown [13]. Impaired respiratory chain activity or failure of mitochondrial function has been implicated in the pathogenesis of several mitochondrial disorders including neurodegenerative disorders [14]
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