Protective effects and mechanism of total coptis alkaloids on A β25–35 induced learning and memory dysfunction in rats

Yang  Zheng-qin; Yang Su-fen; Yang Jun-qing; Zhou Qi-xin; Li Shao-lin

doi:10.1007/s11655-007-0050-8

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Protective effects and mechanism of total coptis alkaloids on A β25–35 induced learning and memory dysfunction in rats

OriginalPaper | Updated：2021-08-27

- Protective effects and mechanism of total coptis alkaloids on A β25–35 induced learning and memory dysfunction in rats
- Protective effects and mechanism of total coptis alkaloids on A β25–35 induced learning and memory dysfunction in rats
- 中国结合医学杂志（英文版） 2007年13卷第1期页码：50-54
- Affiliations：
  
  Department of Nuclear Medicine, Chongqing University of Medical Science,Chongqing,China
- Author bio：
- Funds：
- DOI：10.1007/s11655-007-0050-8
  中图分类号：
- 纸质出版日期：2007，
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Yang, Zq., Yang, Sf., Yang, Jq. et al. Protective effects and mechanism of total coptis alkaloids on A β25–35 induced learning and memory dysfunction in rats., Chin. J Integ. Med. 13, 50–54 (2007). https://doi.org/10.1007/s11655-007-0050-8

Yang Zheng-qin, Yang Su-fen, Yang Jun-qing, et al. Protective effects and mechanism of total coptis alkaloids on A β25–35 induced learning and memory dysfunction in rats[J]. Chinese Journal of Integrative Medicine, 2007,13(1):50-54.
Yang, Zq., Yang, Sf., Yang, Jq. et al. Protective effects and mechanism of total coptis alkaloids on A β25–35 induced learning and memory dysfunction in rats., Chin. J Integ. Med. 13, 50–54 (2007). https://doi.org/10.1007/s11655-007-0050-8 DOI：

Yang Zheng-qin, Yang Su-fen, Yang Jun-qing, et al. Protective effects and mechanism of total coptis alkaloids on A β25–35 induced learning and memory dysfunction in rats[J]. Chinese Journal of Integrative Medicine, 2007,13(1):50-54. DOI： 10.1007/s11655-007-0050-8.

摘要

To observe the effect of total coptis alkaloids (TCA) on β-amyloid peptide (A β25–35) induced learning and memory dysfunction in rats

and to explore its mechanism. Forty male Wistar rats were randomly divided into four groups: the control group

the model group

the TCA low dose (60 mg/kg) group and the TCA high dose (120 mg/kg) group

10 in each. A β25–35 (5 μ l

2 μ g/μ l) was injected into bilateral hippocampi of each rat to induce learning and memory dysfunction. TCA were administered through intragavage for consecutive 15 days. Morris Water Maze test was used to assess the impairment of learning and memory; concentration of malondialdehyde (MDA) in cerebral cortex was determined by thiobarbituric acid reactive substance to indicate the level of lipid peroxidation in brain tissues; activity of manganese-superoxide dismutase (Mn-SOD) in cerebral cortex was determined by xanthine-oxidase to indicate the activity of the enzyme; and NF-κ B protein expression in cerebral cortex was measured by SP immunohistochemistry. (1) Morris Water Maze test showed that

during the 4 consecutive days of acquisition trials

the rats in the model group took longer latency and searching distance than those in the control group (P<0.01)

which could be shortened by high dose TCA (P<0.05); during the spatial probe trial on the fifth day

the rats in the model group took shorter searching time and distance on the previous flat area than those in the control group (P<0.01)

which could be prolonged after TCA treatment (for low dose group

P<0.05; for high dose group

P<0.01). (2) Analysis of cerebral cortical tissues showed that

compared with the control group

MDA level got significantly increased and Mn-SOD activity decreased in the model group (both P<0.01). After having been treated with TCA

the MDA level got significantly decreased (P<0.05 and P<0.01 respectively for low and high dose group)

while relative increase of Mn-SOD activity only appeared in high dose group (P<0.05). (3) Immunohistochemistry analysis showed the protein expression of NF-κ B got significantly increased after modeling

while high dose TCA can significantly inhibit it. TCA could improve A β25–35 induced dysfunction of learning and memory in rats

and its protective mechanism is associated with its actions in decreasing MDA level

increasing Mn-SOD activity and inhibiting the expression of NF-κ B in cerebral cortex.

Abstract

To observe the effect of total coptis alkaloids (TCA) on β-amyloid peptide (A β25–35) induced learning and memory dysfunction in rats

and to explore its mechanism. Forty male Wistar rats were randomly divided into four groups: the control group

the model group

the TCA low dose (60 mg/kg) group and the TCA high dose (120 mg/kg) group

10 in each. A β25–35 (5 μ l

during the 4 consecutive days of acquisition trials

the rats in the model group took longer latency and searching distance than those in the control group (P<0.01)

which could be shortened by high dose TCA (P<0.05); during the spatial probe trial on the fifth day

the rats in the model group took shorter searching time and distance on the previous flat area than those in the control group (P<0.01)

which could be prolonged after TCA treatment (for low dose group

P<0.05; for high dose group

P<0.01). (2) Analysis of cerebral cortical tissues showed that

compared with the control group

MDA level got significantly increased and Mn-SOD activity decreased in the model group (both P<0.01). After having been treated with TCA

the MDA level got significantly decreased (P<0.05 and P<0.01 respectively for low and high dose group)

while high dose TCA can significantly inhibit it. TCA could improve A β25–35 induced dysfunction of learning and memory in rats

and its protective mechanism is associated with its actions in decreasing MDA level

increasing Mn-SOD activity and inhibiting the expression of NF-κ B in cerebral cortex.

关键词

total coptis alkaloidsratβ-amyloid peptidelearning and memory

Keywords

total coptis alkaloidsratβ-amyloid peptidelearning and memory

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