Schisandrin ameliorates cognitive deficits, endoplasmic reticulum stress and neuroinflammation in streptozotocin (STZ)-induced Alzheimer’s disease rats
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- Song Lin
- School of Life Sciences, Huizhou University, 46 Yanda Avenue, Huizhou, Guangdong 516007, P.R. China
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- Piao Zhongyuan
- Department of Neurology, Huizhou Third People’s Hospital, Huizhou Hospital of Guangzhou Medical University, 1 Xuebei Street, Huizhou, Guangdong 516002, P.R. China
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- Yao Lifen
- Department of Neurology, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Harbin, Heilongjiang 150001, P.R. China
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- Zhang Limei
- Department of Obstetrics and Gynecology, Huizhou Third People’s Hospital, Huizhou Hospital of Guangzhou Medical University, 1 Xuebei Street, Huizhou, Guangdong 516002, P.R. China
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- Lu Yichan
- Department of Chinese Medicine, Dalian Maternity and Child Health Care Hospital, 321 Jiefang Road, Dalian, Liaoning 116033, People’s Republic of China
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<p>Schisandrin, an active component extracted from Schisandra chinensis (Turcz.) Baill has been reported to alleviate the cognitive impairment in neurodegenerative disorder like Alzheimer’s disease (AD). However, the mechanism by which schisandrin regulates the cognitive decline is still unclear. In our study, intracerebroventricular injection of streptozotocin (STZ) was employed to establish AD model in male Wistar rats, and indicated dose of schisandrin was further administered. The Morris water maze test was performed to evaluate the ability of learning and memory in rats with schisandrin treatment. The results indicated that schisandrin improved the capacity of cognition in STZ-induced rats. The contents of pro-inflammatory cytokines in brain tissue were determined by ELISA, and the expressions of these cytokines were assessed by western-blot and immunohistochemistry. The results showed that treatment of schisandrin significantly reduced the production of inflammation mediators including tumor necrosis factor-α, interleukin-1β and interleukin-6. Further study suggested a remarkable decrease in the expressions of ER stress maker proteins like C/EBP-homologous protein, glucose-regulated protein 78 and cleaved caspase-12 in the presence of schisandrin, meanwhile the up-regulation of sirtuin 1 (SIRT1) was also observed in the same group. Additionally, the results of western-blot and EMSA demonstrated that schisandrin inhibited NF-κB signaling in the brain of STZ-induced rats. In conclusion, schisandrin ameliorated STZ-induced cognitive dysfunction, ER stress and neuroinflammation which may be associated with up-regulation of SIRT1. Our study provides novel mechanisms for the neuroprotective effect of schisandrin in AD treatment.</p>
収録刊行物
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- Experimental Animals
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Experimental Animals 69 (3), 363-373, 2020
公益社団法人 日本実験動物学会