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PLoS One. 2015 Nov 10;10(11):e0142483. doi: 10.1371/journal.pone.0142483. eCollection 2015.

Schisandrin B Ameliorates ICV-Infused Amyloid β Induced Oxidative Stress and Neuronal Dysfunction through Inhibiting RAGE/NF-κB/MAPK and Up-Regulating HSP/Beclin Expression.

Author information

1
J.K.K. Nattraja College of Pharmacy, Komarapalayam, Tamil Nadu, India.
2
Department of Cardiovascular Sciences, Houston Methodist Research Institute, Houston, Texas, United States of America.
3
Department of Clinical Pharmacology, Niigata University of Pharmacy & Applied Life Sciences (NUPALS), Niigata City, Japan.
4
Division of Neurobiology, Brain Research Institute, Niigata University, Niigata, Japan.
5
Department of Gastroenterology and Hepatology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
6
Section of Biochemistry and Cell biology, Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong SAR, China.
7
Basic studies on second generation functional foods, NUPALS, NUPALS Liaison R/D promotion division, Niigata, Japan, Changchun University of Chinese Medicine, Changchun, RP China.

Abstract

Amyloid β (Aβ)-induced neurotoxicity is a major pathological mechanism of Alzheimer's disease (AD). Our previous studies have demonstrated that schisandrin B (Sch B), an antioxidant lignan from Schisandra chinensis, could protect mouse brain against scopolamine- and cisplatin-induced neuronal dysfunction. In the present study, we examined the protective effect of Sch B against intracerebroventricular (ICV)-infused Aβ-induced neuronal dysfunction in rat cortex and explored the potential mechanism of its action. Our results showed that 26 days co-administration of Sch B significantly improved the behavioral performance of Aβ (1-40)-infused rats in step-through test. At the same time, Sch B attenuated Aβ-induced increases in oxidative and nitrosative stresses, inflammatory markers such as inducible nitric oxide syntheses, cyclooxygenase-2, interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α, and DNA damage. Several proteins such as receptor for advanced glycation end products (RAGE), nuclear factor-κB, mitogen-activated protein kinases, and apoptosis markers were over expressed in Aβ-infused rats but were significantly inhibited by Sch B treatment. Furthermore, Sch B negatively modulated the Aβ level with simultaneous up-regulation of HSP70 and beclin, autophagy markers in Aβ-infused rats. The aforementioned effects of Sch B suggest its protective role against Aβ-induced neurotoxicity through intervention in the negative cycle of RAGE-mediated Aβ accumulation during AD patho-physiology.

PMID:
26556721
PMCID:
PMC4640572
DOI:
10.1371/journal.pone.0142483
[Indexed for MEDLINE]
Free PMC Article

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