[Effect of qingxin kaiqiao recipe saponin on the expressions of Bax, Bcl-2, Abeta, and betaAPP in the cortex and hippocampus of Alzheimer's disease rats]

Zhongguo Zhong Xi Yi Jie He Za Zhi. 2012 Sep;32(9):1258-63.
[Article in Chinese]

Abstract

Objective: To study the effects of Qingxin Kaiqiao Recipe (QKR) saponin on the expressions of Bax, Bcl-2, beta-amyloid (Abeta), and beta-amyloid precursor protein (betaAPP) in the cortex and hippocampus of Alzheimer's disease (AD) rats.

Methods: Thirty-two SD rats of SPF grade were selected. Abeta 25 - 35 was injected into the bilateral amygdala to prepare the AD model. After modeling rats were randomly divided into the model group, the donepezil hydrochloride group (Donepezil Hydrochloride Tablet, 1.67 mg/kg), the QLR group (QLR Decoction, 12.67 mL/kg), and the saponin group (saponin, 6.30 mg/kg), 8 rats in each group. Another 8 rats were selected as the normal group. Rats in the normal group and the model group were given with equal volume of double distilled water by gastrogavage. The intervention was performed once daily for 2 successive weeks. The Morris water maze test was carried out by the end of medication. The escape latency and the platform crossing times were recorded during the 1 -5 days. The expressions of Bax, Bcl-2, Abeta, and betaAPP in the cortex and hippocampus were detected using immunohistochemical assay.

Results: Compared with the model group, the 3rd - 5th day escape latency were all shortened in each medication group. The expressions of Bax, Abeta, and betaAPP decreased in the cortex and hippocampus. The numbers of platform crossing increased. The expression of Bcl-2 in the cortex increased. The expression of Bcl-2 in the hippocampus increased in the donepezil hydrochloride group and the QLR group with statistical difference (P<0.01, P<0.05). Compared with the donepezil hydrochloride group, the expression of betaAPP increased in the cortex and hippocampus of the saponin group. The expression of Abeta in the cortex and hippocampus decreased, the expression of Bax in the hippocampus decreased, and the expression of Bcl-2 in the cortex increased in the QLR group. The escape latency was obviously postponed at day 3 -5, the platform crossing times decreased, the expression of Bcl-2 in the cortex and hippocampus decreased in the saponin group, showing statistical difference (P<0.05, P<0.01).

Conclusion: QKR could significantly improve AD rats' learning, memory, and spatial capabilities, which might be achieved through decreasing the expressions of Bax, Abeta, and betaAPP in the cerebral cortex and hippocampus, and elevating the expression of Bcl-2.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / drug therapy
  • Alzheimer Disease / metabolism*
  • Amyloid beta-Peptides / metabolism
  • Amyloid beta-Protein Precursor / metabolism
  • Animals
  • Cerebral Cortex / drug effects
  • Cerebral Cortex / metabolism*
  • Drugs, Chinese Herbal / pharmacology*
  • Hippocampus / drug effects
  • Hippocampus / metabolism*
  • Male
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Saponins / pharmacology*
  • bcl-2-Associated X Protein / metabolism

Substances

  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor
  • Bax protein, rat
  • Drugs, Chinese Herbal
  • Proto-Oncogene Proteins c-bcl-2
  • Saponins
  • bcl-2-Associated X Protein