Berberine modulates amyloid-β peptide generation by activating AMP-activated protein kinase. (October 2017)
- Record Type:
- Journal Article
- Title:
- Berberine modulates amyloid-β peptide generation by activating AMP-activated protein kinase. (October 2017)
- Main Title:
- Berberine modulates amyloid-β peptide generation by activating AMP-activated protein kinase
- Authors:
- Zhang, Haijing
Zhao, Chunhui
Cao, Guoqiong
Guo, Limin
Zhang, Shuai
Liang, Yuexia
Qin, Chunxia
Su, Ping
Li, Hang
Zhang, Wensheng - Abstract:
- Abstract: Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by memory deficits and cognitive decline. Excessive amyloid-β (Aβ) peptide aggregates and forms soluble oligomers and insoluble cerebral amyloid plaques, which is widely thought to be the underlying pathogenic mechanism of AD. Therefore, effective regulation of Aβ metabolism is an important aspect of preventing and improving AD. Berberine, which is the main active component of the traditional medicinal herb Coptidis rhizoma, has a positive effect on reducing Aβ levels. However, the exact mechanism involved is unclear and requires more investigation. In the present study, we examined the role of berberine in the activation of AMP-activated protein kinase (AMPK) in neuroblastoma cells and primary cultured neurons and sought to characterize the role of AMPK in the metabolism of Aβ. The results indicate that berberine reduces Aβ generation and decreases the expression of β-site APP cleaving enzyme-1 (BACE1) via activating AMPK in N2a mouse neuroblastoma cells stably expressing human Swedish mutant APP695 (N2a/APP695sw), N2a cells, and primary cultured cortical neurons. Therefore, berberine reduced the accumulation of Aβ, which likely contributes to its memory enhancing effect in patients with AD. Highlights: Berberine activates AMPK in neuroblastoma cells and neurons. Berberine reduces Aβ generation in neuroblastoma cells and neurons. Berberine decreases the expression of BACE1 viaAbstract: Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by memory deficits and cognitive decline. Excessive amyloid-β (Aβ) peptide aggregates and forms soluble oligomers and insoluble cerebral amyloid plaques, which is widely thought to be the underlying pathogenic mechanism of AD. Therefore, effective regulation of Aβ metabolism is an important aspect of preventing and improving AD. Berberine, which is the main active component of the traditional medicinal herb Coptidis rhizoma, has a positive effect on reducing Aβ levels. However, the exact mechanism involved is unclear and requires more investigation. In the present study, we examined the role of berberine in the activation of AMP-activated protein kinase (AMPK) in neuroblastoma cells and primary cultured neurons and sought to characterize the role of AMPK in the metabolism of Aβ. The results indicate that berberine reduces Aβ generation and decreases the expression of β-site APP cleaving enzyme-1 (BACE1) via activating AMPK in N2a mouse neuroblastoma cells stably expressing human Swedish mutant APP695 (N2a/APP695sw), N2a cells, and primary cultured cortical neurons. Therefore, berberine reduced the accumulation of Aβ, which likely contributes to its memory enhancing effect in patients with AD. Highlights: Berberine activates AMPK in neuroblastoma cells and neurons. Berberine reduces Aβ generation in neuroblastoma cells and neurons. Berberine decreases the expression of BACE1 via activating AMPK. … (more)
- Is Part Of:
- Neuropharmacology. Volume 125(2017)
- Journal:
- Neuropharmacology
- Issue:
- Volume 125(2017)
- Issue Display:
- Volume 125, Issue 2017 (2017)
- Year:
- 2017
- Volume:
- 125
- Issue:
- 2017
- Issue Sort Value:
- 2017-0125-2017-0000
- Page Start:
- 408
- Page End:
- 417
- Publication Date:
- 2017-10
- Subjects:
- Alzheimer's disease -- Berberine -- AMP-activated protein kinase -- Amyloid-β -- β-site APP cleaving enzyme-1
AD Alzheimer's disease -- Aβ Amyloid-β -- APP Amyloid precursor protein -- AMPK AMP-activated protein kinase -- BACE1 β-site APP cleaving enzyme-1 -- β-CTF β-C-terminal fragment -- IDE Insulin degrading enzyme -- RAGE Receptor for advanced glycation end products
Neuropsychopharmacology -- Periodicals
Autonomic Agents -- Periodicals
Neuropsychopharmacologie -- Périodiques
Neuropsychopharmacology
Periodicals
Electronic journals
615.78 - Journal URLs:
- http://www.sciencedirect.com/science/journal/00283908 ↗
http://www.elsevier.com/journals ↗ - DOI:
- 10.1016/j.neuropharm.2017.08.013 ↗
- Languages:
- English
- ISSNs:
- 0028-3908
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 6081.517500
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