Neutroprotective efficacy of sodium tanshinone B on hippocampus neuron in a rat model of focal cerebral ischemia

Qing Cai; Hong-wu Wang; Sheng-yu Hua; Jun-zhen Tan; Tao Zhou; Chun-shen Li

doi:10.1007/s11655-012-1266-9

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Neutroprotective efficacy of sodium tanshinone B on hippocampus neuron in a rat model of focal cerebral ischemia

OriginalPaper | Updated：2021-08-27

- Neutroprotective efficacy of sodium tanshinone B on hippocampus neuron in a rat model of focal cerebral ischemia
- Neutroprotective efficacy of sodium tanshinone B on hippocampus neuron in a rat model of focal cerebral ischemia
- 中国结合医学杂志（英文版） 2012年18卷第11期页码：837-845
- Affiliations：
  
  1. Department of Physiology, Tianjin University of Traditional Chinese Medicine,Tianjin,China
  2. College of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine,Tianjin,China
  3. Department of Experiment, Tianjin University of Traditional Chinese Medicine,Tianjin,China
- Author bio：
- Funds：
  
  Supported by Science Development Foundation of Tianjin Institute of Education (No. 20070301) and Tianjin Natural Science Foundation of China (No. 11JCYBJC13400)
- DOI：10.1007/s11655-012-1266-9
  中图分类号：
- 纸质出版日期：2012，
  
  网络出版日期：2012-10-20，
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Cai, Q., Wang, Hw., Hua, Sy. et al. Neutroprotective efficacy of sodium tanshinone B on hippocampus neuron in a rat model of focal cerebral ischemia., Chin. J. Integr. Med. 18, 837–845 (2012). https://doi.org/10.1007/s11655-012-1266-9

Qing Cai, Hong-wu Wang, Sheng-yu Hua, et al. Neutroprotective efficacy of sodium tanshinone B on hippocampus neuron in a rat model of focal cerebral ischemia[J]. Chinese Journal of Integrative Medicine, 2012,18(11):837-845.
Cai, Q., Wang, Hw., Hua, Sy. et al. Neutroprotective efficacy of sodium tanshinone B on hippocampus neuron in a rat model of focal cerebral ischemia., Chin. J. Integr. Med. 18, 837–845 (2012). https://doi.org/10.1007/s11655-012-1266-9 DOI：

Qing Cai, Hong-wu Wang, Sheng-yu Hua, et al. Neutroprotective efficacy of sodium tanshinone B on hippocampus neuron in a rat model of focal cerebral ischemia[J]. Chinese Journal of Integrative Medicine, 2012,18(11):837-845. DOI： 10.1007/s11655-012-1266-9.

摘要

To investigate the protective effects of sodium tanshinone B (STB) on brain damage following focal ischemia-reperfusion (I/R) injury through interfering with N-methyl-D-aspartic acid receptor (NMDAR) and excitatory and inhibitory amino acids

and evaluate the potential mechanisms of the neuroprotective activity of STB. Transient forebrain ischemia was induced by middle cerebral artery occlusion (MCAO). The rats were randomized into a sham operated group

a model group (I/R) and three STB different dose groups. Rats were pretreated with STB at the doses of 4

16 mg/kg (STB1

STB2

STB3) for 3 days before MCAO. The expression of NMDAR1 was detected by immunohistochemistry and Western blotting. The concentrations of glutamate and γ-aminobutyric acid (GABA) were analyzed using high performance liquid chromatography. STB treatment reduced neurological defect scores

cerebral infarction volume and brain water content. The levels of NMDAR1 were significantly higher in the l/R and STB1 groups than that of the sham and the STB3 groups (P<0.01). Optical density of NMDAR1 was significantly increased in cornu ammonis (CA)1 region of the l/R group (P<0.05). STB treatment reduced NMDAR1 optical density in the CA1 region (P<0.01). The levels of glutamate were significantly lower in the hippocampus in the STB3 group than that of the l/R

STB1 and STB2 groups (P<0.01). Preconditioning with STB appears to be a simple and promising strategy to reduce or even prevent cerebral l/R injury and has potential for future clinical application.

Abstract

a model group (I/R) and three STB different dose groups. Rats were pretreated with STB at the doses of 4

16 mg/kg (STB1

STB2

STB1 and STB2 groups (P<0.01). Preconditioning with STB appears to be a simple and promising strategy to reduce or even prevent cerebral l/R injury and has potential for future clinical application.

关键词

ischemia/reperfusion injuryN-methyl-D-Aspartic acid receptorhippocampusCa2+sodium tanshinone

Keywords

ischemia/reperfusion injuryN-methyl-D-Aspartic acid receptorhippocampusCa2+sodium tanshinone

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