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6-Paradol and its glucoside improve memory disorder in mice
- Source :
- Food & Function. 11:9892-9902
- Publication Year :
- 2020
- Publisher :
- Royal Society of Chemistry (RSC), 2020.
-
Abstract
- In this study, the effects of 6-paradol (6P) and 6-paradol-β-glucoside (6PG) on neuritogenesis were investigated using PC12 cells. Treatment with 200 μM 6P or 6PG and nerve growth factor (NGF) (5 ng mL-1) increased the number of elongated dendritic cells 8.7 and 5.4 times, respectively, compared to that with NGF (5 ng mL-1) treatment alone. 6P and 6PG did not stimulate the phosphorylation of extracellular regulated protein kinases (ERK)1/2 and cAMP response element-binding protein (CREB) in the tropomyosin receptor kinase A (TrkA) pathway as their activities were suppressed by the pathway inhibitor, k252a. 6P enhanced Ca2+ influx into the cells, whereas 6PG had no effect on Ca2+ influx, although it stimulated PC12 cell differentiation. High-performance liquid chromatography (HPLC) analysis of 6PG in PC12 culture medium suggested that 6PG was deglycosylated to generate 6P, which exhibited the effect. Furthermore, the bioactivities of 6P and 6PG were investigated in mice, and the results revealed that they ameliorated short-term memory loss in animals during behavioral testing.
- Subjects :
- Male
0301 basic medicine
MAPK/ERK pathway
Cellular differentiation
Tropomyosin receptor kinase A
CREB
PC12 Cells
Mice
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Glucosides
Memory
Zingiberaceae
Animals
Humans
Phosphorylation
Receptor, trkA
Cyclic AMP Response Element-Binding Protein
Memory Disorders
biology
Plant Extracts
Kinase
Chemistry
Guaiacol
General Medicine
Ketones
Molecular biology
Rats
030104 developmental biology
Nerve growth factor
030220 oncology & carcinogenesis
Seeds
biology.protein
Calcium
Paradol
K252a
Signal Transduction
Food Science
Subjects
Details
- ISSN :
- 2042650X and 20426496
- Volume :
- 11
- Database :
- OpenAIRE
- Journal :
- Food & Function
- Accession number :
- edsair.doi.dedup.....f12d9724364db7ece51d623c54a8e04a