ReferenceID 5098
The protective effects of moscatilin against methylglyoxal-induced neurotoxicity via the regulation of p38/JNK MAPK pathways in PC12 neuron-like cells
Food Chem Toxicol
Methylglyoxal (MGO) is an endogenous toxic compound that plays a vital role in diabetic complications such as diabetic neuropathy. Moscatilin is a bibenzyl component from Dendrobium species, has been shown to possess a w
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Record Fields
Scalar fields from the final reference record.
- Reference Id
- 5098
- Evidence Id
- 21688
- Core Evidence Id
- 21688
- Source Reference Id
- 3485
- Herb2 Reference Id
- HBREF004282
- Subject Paper Key
- HBIN023302_32325188
- Pubmed Id
- 32325188
- Doi
- 10.1016/j.fct.2020.111369
- Paper Title
- The protective effects of moscatilin against methylglyoxal-induced neurotoxicity via the regulation of p38/JNK MAPK pathways in PC12 neuron-like cells
- Paper Abstract
- Methylglyoxal (MGO) is an endogenous toxic compound that plays a vital role in diabetic complications such as diabetic neuropathy. Moscatilin is a bibenzyl component from Dendrobium species, has been shown to possess a wide range of pharmacological activities. To clarify whether moscatilin prevents rat pheochromocytoma cells (PC12 cells) from damage induced by MGO, cells were pre-treated with moscatilin and then stimulated with MGO. Moscatilin inhibited MGO associated cytotoxicity in a concentration (0.1, 0.5, or 1.0 mumol/L)-dependent manner and downregulated the formation of advanced glycation end products and reactive oxygen species. Moscatilin attenuated MGO-induced mitochondrial dysfunction involving the loss of mitochondrial membrane potential and depletion of adenosine triphosphate. MGO induced cell apoptosis via the upregulation of p53, caspases 3 and poly(ADP-ribose)polymerase, enhancement of cytochrome c release, and interruption of the Bax/Bcl-2 balance; these detrimental effects were ameliorated by moscatilin. Furthermore, moscatilin inhibited MGO-induced activation of MAP kinase (MAPK) superfamily, including p38 and c-Jun N-terminal kinases (JNKs). In conclusion, we found that the neuroprotective effect of moscatilin is due to a reduction of MGO-induced damage to mitochondria function through modulating the p38 and JNK stress-activated MAPK cascades pathway. Thus, it might be a potent compound for preventing/counteracting diabetic neuropathy.
- Journal
- Food Chem Toxicol
- Publish Year
- 2020
- Experiment Subject
- rat; pc12 cells
- Experiment Type
- Cell Experiment
- Phenotype Related
- Pheochromocytoma; Mitochondrial Dysfunction; Diabetic Neuropathy; Diabetic Complications
- Paper Title Cn
- Paper Title En
- The protective effects of moscatilin against methylglyoxal-induced neurotoxicity via the regulation of p38/JNK MAPK pathways in PC12 neuron-like cells
- Bilingual Status
- semi_complete