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Objective   To investigate the effects of QKF on expression of amyloid-beta (A β ), interleukin-1 beta (IL-1 β ), 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 (A β ) 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 A β , IL-1 β , 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 A β , IL-1 β , 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 A β , IL-1 β , 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.

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

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