Journal
PHARMACEUTICALS
Volume 15, Issue 5, Pages -Publisher
MDPI
DOI: 10.3390/ph15050627
Keywords
autophagy; Parkinson's; glutamate toxicity; neurodegeneration; neuroprotection
Categories
Funding
- 90th Anniversary of Chulalongkorn University Scholarship
- Rachadapisek Sompot Fund [CU_GR_63-82-37-09]
- Thailand Research Fund (TRF)/Chulalongkorn University (CU) joint support through the Royal Golden Jubilee Ph.D. (RGJPHD) Program [PHD/0003/2555]
- Thailand Research Fund (TRF)/Chulalongkorn University (CU) joint support through Newton fund Ph.D
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In this study, Rhinacanthin-C and -D were isolated from Rhinacanthus nasustus, and their neuroprotective effects against glutamate-induced apoptosis in HT-22 cells were investigated. It was found that Rhinacanthin-C inhibited autophagy and increased ER stress, while low concentrations of Rhinacanthin-C prevented ER stress and CHOP expression. All concentrations of Rhinacanthin-C prevented ROS production and ERK1/2 phosphorylation.
Neurodegenerative diseases present an increasing problem as the world's population ages; thus, the discovery of new drugs that prevent diseases such as Alzheimer's, and Parkinson's diseases are vital. In this study, Rhinacanthin-C and -D were isolated from Rhinacanthus nasustus, using ethyl acetate, followed by chromatography to isolate Rhinacanthin-C and -D. Both compounds were confirmed using NMR and ultra-performance-LCMS. Using glutamate toxicity in HT-22 cells, we measured cell viability and apoptosis, ROS build-up, and investigated signaling pathways. We show that Rhinacanthin-C and 2-hydroxy-1,4-naphthoquinone have neuroprotective effects against glutamate-induced apoptosis in HT-22 cells. Furthermore, we see that Rhinacanthin-C resulted in autophagy inhibition and increased ER stress. In contrast, low concentrations of Rhinacanthin-C and 2-hydroxy-1,4-naphthoquinone prevented ER stress and CHOP expression. All concentrations of Rhinacanthin-C prevented ROS production and ERK1/2 phosphorylation. We conclude that, while autophagy is present in HT-22 cells subjected to glutamate toxicity, its inhibition is not necessary for cryoprotection.
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