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Home > Archive>Volume 32, Issue 10, 2022 >78-90. DOI:10. 3969 / j.issn.1671-7856. 2022. 10. 010
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Therapeutic effect and mechanisms of Kaixin San in AD rats induced by bilateral Aβ1-42 injection into the CA1 area of the hippocampus
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1. School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 102488, China.2. Beijing Tongrentang Research Institute, Beijing 100071. 3. Beijing Institute for Drug Control, Beijing 102200

Clc Number:

R-33

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    Abstract:

    To examine the therapeutic effect of Kaixin San in rats with AD caused by bilateral Aβ1-42 injection into CA1 area of the hippocampus, and to preliminarily clarify its mechanisms. Methods Using the “β-amyloid protein toxicity theory”, the rat model of AD was established by bilaterally injecting Aβ1-42 oligopeptide segments in the CA1 region of the hippocampus of SD rats using a brain stereotaxic instrument. The rats were randomly divided into model, Hupezine A, Kaixin San low, middle and high dose groups, with 10 rats in each group. Another 10 rats were subjected to intracranial injection of an equal amount of physiological saline as the sham operation group and 10 normal rats were used as the blank control. The rats were subjected to continuous intragastric administrations for 30 days. Changes in learning and memory performance were observed by the Morris water maze behavioral test. HE and Nissl staining was used to visualize pathological morphology of the brain. The contents of cholinergic neurotransmitters ( ACh, AChE and ChAT ), proinflammatory factors (TNF-α, IL-6 and IL-1β), and β-amyloid protein (APP, Aβ1-40 and Aβ1-42 ) in brain tissue were measured by ELISA. Expression of tau protein and GSK-3β in cortical and hippocampal tissues was detected by IHC. BAX and BCL-2 expression in brain tissues was measured by Western blot. Results Compared with the model group, rats in the Kaixin San treatment groups had a significantly shorter escape latency, an increased number of platform crossings, and an enhanced dwell time and percentage of swimming distance to the total distance in the target quadrant (P<0. 05 or P<0. 01). The numbers of neurons in cortical and hippocampal tissues were increased, the morphological structure tended to be normalized, the number of Nissl bodies increased, and the cytoplasm darkened. AChE activity was attenuated, and ChAT with ACh levels were significantly increased in brain tissue (P<0. 05 or P<0. 01). TNF-α, IL-6, IL-1β, APP,Aβ1-40 and Aβ1-42 contents were decreased markedly (P<0. 05 or P<0. 01). Expression of tau protein and GSK-3β in both cortical and hippocampal tissues was downregulated (P<0. 05 or P<0. 01). BAX protein expression decreased, and the ratio of BCL-2/ BAX tended to increase to various degrees (P>0. 05). Conclusions Kaixin San has a good therapeutic effect on dementia symptoms and brain tissue damage in AD-injured rats, and its mechanisms involve the repair of the cholinergic system, inhibition of proinflammatory factor release, clearance of β-amyloid protein, and regulation of tau protein phosphorylation.

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History
  • Received:December 29,2021
  • Online: May 08,2023
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