ReferenceID 6135
Sulforaphene Ameliorates Neuroinflammation and Hyperphosphorylated Tau Protein via Regulating the PI3K/Akt/GSK-3 β Pathway in Experimental Models of Alzheimer's Disease
Oxid Med Cell Longev
Alzheimer's disease (AD) is the most common form of dementia characterized by progressive loss of cognitive functions due to neuronal death mainly in the hippocampal and cortical brain. Sulforaphene (SF) is one of the ma
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- Reference Id
- 6135
- Evidence Id
- 22725
- Core Evidence Id
- 22725
- Source Reference Id
- 5531
- Herb2 Reference Id
- HBREF006328
- Subject Paper Key
- HBIN041943_32963694
- Pubmed Id
- 32963694
- Doi
- 10.1155/2020/4754195
- Paper Title
- Sulforaphene Ameliorates Neuroinflammation and Hyperphosphorylated Tau Protein via Regulating the PI3K/Akt/GSK-3 β Pathway in Experimental Models of Alzheimer's Disease
- Paper Abstract
- Alzheimer's disease (AD) is the most common form of dementia characterized by progressive loss of cognitive functions due to neuronal death mainly in the hippocampal and cortical brain. Sulforaphene (SF) is one of the main isothiocyanates isolated from a Chinese herb Raphani Semen. In this study, we aimed to investigate the neuroprotective effects of SF using in vitro and in vivo models of AD. Streptozotocin (STZ) was intracranially injected into the rats; then, SF (25 and 50 mg/kg) was given orally once a day for 6 consecutive weeks. After drug treatment, the cognitive functions were assessed using the Morris Water Maze Test (MWMT). After the MWMT, the rats were euthanized and brain tissues were collected. In the in vitro test, BV-2 microglia were pretreated with SF (1 and 2 muM) for 1 h and then stimulated with lipopolysaccharide (LPS) for another 23 h. Both molecular and histological methods were used to unravel the action mechanisms and elucidate the signaling pathway. The MWMT results showed that SF treatment significantly improved the STZ-induced cognitive deficits in rats. SF treatment markedly suppressed the production of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) but increased the release of IL-10 in the STZ-treated rats. In addition, SF significantly inhibited the phosphorylation of tau protein at Thr205, Ser396, and Ser404 sites, while enhancing the ratios of p-Akt (Ser473)/Akt and p-GSK-3beta (Ser9)/GSK-3beta in the hippocampus of the STZ-treated rats. On the other hand, SF (1 and 2 muM) treatment also markedly attenuated the cytotoxicity induced by LPS in BV-2 cells. In addition, SF treatment obviously suppressed the releases of nitric oxide (NO), TNF-alpha, and IL-6 in the LPS-stimulated BV-2 cells. Moreover, SF treatment significantly mitigated the nuclear translocation of p-NF-kappaB p65 and the ratio of p-GSK-3beta (Ser9)/GSK-3beta in LPS-stimulated BV-2 cells. Taken together, SF possessed neuroprotective effects against the STZ-induced cognitive deficits in rats and LPS-induced neuroinflammation in BV-2 cells via modulation of the PI3K/Akt/GSK-3beta pathway and inhibition of the NF-kappaB activation, suggesting that SF is a promising neuroprotective agent worthy of further development into AD treatment.
- Journal
- Oxid Med Cell Longev
- Publish Year
- 2020
- Experiment Subject
- rat; bv-2 cells; lps-stimulated bv-2 cells
- Experiment Type
- Animal & Cell Experiment
- Phenotype Related
- Alzheimer's Disease; Tumor; Neuronal Death; Cognitive Deficits; Dementia
- Paper Title Cn
- Paper Title En
- Sulforaphene Ameliorates Neuroinflammation and Hyperphosphorylated Tau Protein via Regulating the PI3K/Akt/GSK-3 β Pathway in Experimental Models of Alzheimer's Disease
- Bilingual Status
- semi_complete