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Bushen‑Yizhi formula ameliorates cognition deficits and attenuates oxidative stress‑related neuronal apoptosis in scopolamine‑induced senescence in mice

  • Authors:
    • Xue‑Qin Hou
    • Dian‑Wei Wu
    • Chun‑Xia Zhang
    • Rong Yan
    • Cong Yang
    • Cui‑Ping  Rong
    • Lei Zhang
    • Xiang Chang
    • Ru‑Yu Su
    • Shi‑Jie Zhang
    • Wen‑Qing  He
    • Zhao  Qu
    • Shi Li
    • Zi‑Ren Su
    • Yun‑Bo Chen
    • Qi Wang
    • Shu‑Huan Fang
  • View Affiliations / Copyright

    Affiliations: Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China, Shantou Hospital of Traditional Chinese Medicine, Guangzhou, Guangdong 515031, P.R. China, School of Chinese Materia Medica, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China
    Copyright: © Hou et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].
  • Pages: 429-439
    |
    Published online on: June 11, 2014
       https://doi.org/10.3892/ijmm.2014.1801
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Abstract

Bushen‑Yizhi formula (BSYZ), a traditional Chinese medicine formula consisting of six herbs has been reported to possess a neuroprotective effect. The present study aimed to investigate the effects of BSYZ on learning and memory abilities, as well as oxidative stress and neuronal apoptosis in the hippocampus of scopolamine (SCOP)‑induced senescence in mice, in order to reveal whether BSYZ is a potential therapeutic agent for Alzheimer's disease (AD). A high‑performance liquid chromatography (HPLC) fingerprint was applied to provide a chemical profile of BSYZ. Extracts of BSYZ were orally administered to mice with SCOP‑induced memory impairment for two weeks. The learning and memory abilities were determined by the Morris water maze test. The oxidant stress‑related indices, such as activity of superoxide dismutase (SOD) and levels of glutathione (GSH) and malondialdehyde (MDA) were examined in hippocampus of SCOP‑treated mice. The cell death ratio was assessed by TUNEL staining, while apoptotic‑related proteins including Bcl‑2 and Bax were determined by immuno­fluorescent staining and western blot analysis. Caspase‑3 was determined by western blot analysis. Consequently, a chromatographic condition, which was conducted at 35˚C with a flow rate of 0.8 ml/min on the Gemini C18 column with mobile phase of acetonitrile and water‑phosphoric acid (100:0.1, v/v), was established to yield common fingerprint chromatography under 203 nm with a similarity index of 0.986 within 10 batches of BSYZ samples. BSYZ at a dose of 2.92 g/kg significantly improved the cognitive ability, restored the abnormal activity of SOD and increased the levels of MDA and GSH induced by SCOP. Moreover, the neural apoptosis in the hippocampus of SCOP‑treated mice was reversed by BSYZ by regulating the expression of Bcl‑2, Bax and caspase‑3. The results demonstrated that BSYZ had neuroprotective effects in SCOP‑induced senescence in mice by ameliorating oxidative stress and neuronal apoptosis in the brain, supporting its potential in AD treatment.
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Copy and paste a formatted citation
Spandidos Publications style
Hou XQ, Wu DW, Zhang CX, Yan R, Yang C, Rong CP, Zhang L, Chang X, Su RY, Zhang SJ, Zhang SJ, et al: Bushen‑Yizhi formula ameliorates cognition deficits and attenuates oxidative stress‑related neuronal apoptosis in scopolamine‑induced senescence in mice. Int J Mol Med 34: 429-439, 2014.
APA
Hou, X., Wu, D., Zhang, C., Yan, R., Yang, C., Rong, C. ... Fang, S. (2014). Bushen‑Yizhi formula ameliorates cognition deficits and attenuates oxidative stress‑related neuronal apoptosis in scopolamine‑induced senescence in mice. International Journal of Molecular Medicine, 34, 429-439. https://doi.org/10.3892/ijmm.2014.1801
MLA
Hou, X., Wu, D., Zhang, C., Yan, R., Yang, C., Rong, C., Zhang, L., Chang, X., Su, R., Zhang, S., He, W., Qu, Z., Li, S., Su, Z., Chen, Y., Wang, Q., Fang, S."Bushen‑Yizhi formula ameliorates cognition deficits and attenuates oxidative stress‑related neuronal apoptosis in scopolamine‑induced senescence in mice". International Journal of Molecular Medicine 34.2 (2014): 429-439.
Chicago
Hou, X., Wu, D., Zhang, C., Yan, R., Yang, C., Rong, C., Zhang, L., Chang, X., Su, R., Zhang, S., He, W., Qu, Z., Li, S., Su, Z., Chen, Y., Wang, Q., Fang, S."Bushen‑Yizhi formula ameliorates cognition deficits and attenuates oxidative stress‑related neuronal apoptosis in scopolamine‑induced senescence in mice". International Journal of Molecular Medicine 34, no. 2 (2014): 429-439. https://doi.org/10.3892/ijmm.2014.1801
Copy and paste a formatted citation
x
Spandidos Publications style
Hou XQ, Wu DW, Zhang CX, Yan R, Yang C, Rong CP, Zhang L, Chang X, Su RY, Zhang SJ, Zhang SJ, et al: Bushen‑Yizhi formula ameliorates cognition deficits and attenuates oxidative stress‑related neuronal apoptosis in scopolamine‑induced senescence in mice. Int J Mol Med 34: 429-439, 2014.
APA
Hou, X., Wu, D., Zhang, C., Yan, R., Yang, C., Rong, C. ... Fang, S. (2014). Bushen‑Yizhi formula ameliorates cognition deficits and attenuates oxidative stress‑related neuronal apoptosis in scopolamine‑induced senescence in mice. International Journal of Molecular Medicine, 34, 429-439. https://doi.org/10.3892/ijmm.2014.1801
MLA
Hou, X., Wu, D., Zhang, C., Yan, R., Yang, C., Rong, C., Zhang, L., Chang, X., Su, R., Zhang, S., He, W., Qu, Z., Li, S., Su, Z., Chen, Y., Wang, Q., Fang, S."Bushen‑Yizhi formula ameliorates cognition deficits and attenuates oxidative stress‑related neuronal apoptosis in scopolamine‑induced senescence in mice". International Journal of Molecular Medicine 34.2 (2014): 429-439.
Chicago
Hou, X., Wu, D., Zhang, C., Yan, R., Yang, C., Rong, C., Zhang, L., Chang, X., Su, R., Zhang, S., He, W., Qu, Z., Li, S., Su, Z., Chen, Y., Wang, Q., Fang, S."Bushen‑Yizhi formula ameliorates cognition deficits and attenuates oxidative stress‑related neuronal apoptosis in scopolamine‑induced senescence in mice". International Journal of Molecular Medicine 34, no. 2 (2014): 429-439. https://doi.org/10.3892/ijmm.2014.1801
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