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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.

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


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.

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