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Evidence-Based Complementary and Alternative Medicine
Volume 2018, Article ID 9267653, 7 pages
Research Article

Effect of Qingxin Kaiqiao Fang on Hippocampus mRNA Expression of the Inflammation-Related Genes IL-1β, GFAP, and Aβ in an Alzheimer’s Disease Rat Model

1The Second Clinical College, Wenzhou Medical University, Wenzhou 325003, China
2The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, 109 Xue Yuan Xi Road, Lu Cheng District, Wenzhou 325000, China

Correspondence should be addressed to Hai-Yan Hu; moc.361@kyzxdkyzw

Received 24 August 2017; Accepted 18 January 2018; Published 18 February 2018

Academic Editor: Darren R. Williams

Copyright © 2018 Dan-Dan Mao et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Objective. To investigate the effects of QKF on expression of amyloid-beta (Aβ), interleukin-1 beta (IL-1β), and glial fibrillary acidic protein (GFAP) using a rat model of AD. Materials and Methods. Fifty-six male Sprague-Dawley rats were randomly divided into seven groups (eight rats each): control group, sham-operated group, AD model group, groups of AD rats administered with low, medium, and high doses of QKF, and the donepezil group. AD was established by bilateral injection of β-amyloid (Aβ) 1–40 into the hippocampus. Two days after AD was established, drugs were administered by gavage. After 14 days of treatment, we used RT-PCR, Western blotting, and immunohistochemistry to measure the transcript expression and protein abundance of Aβ, IL-1β, and GFAP, and methenamine silver staining was used to detect amyloid protein particle deposition. Results. Compared to the control group, the rats from the AD model group showed significantly greater expression levels of Aβ, IL-1β, and GFAP. However, these differences in expression were abolished by treatment with QKF or donepezil. Conclusion. QKF possesses therapeutic potential against AD because it downregulated Aβ, IL-1β, and GFAP in the hippocampus of AD rats. Future studies should further examine the mechanisms through which QKF produces its effects and the consequences of long-term QKF administration.