Inhibitory effect of tetramethylpyrazine preconditioning on overload training-induced myocardial apoptosis in rats

Yi Yang; Zhang-hua Li; Hua Liu; Wu-di Shi; Jie Zhang

doi:10.1007/s11655-014-1752-3

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Inhibitory effect of tetramethylpyrazine preconditioning on overload training-induced myocardial apoptosis in rats

Updated：2021-08-27

- Inhibitory effect of tetramethylpyrazine preconditioning on overload training-induced myocardial apoptosis in rats
- Chinese Journal of Integrative Medicine Vol. 21, Issue 6, Pages: 423-430(2015)
- Affiliations：
  
  1. College of Health Science, Wuhan Institute of Physical Education,Wuhan,China
  2. Renmin Hospital, Wuhan University,Wuhan,China
  3. Graduate Department, Wuhan Institute of Physical Education,Wuhan,China
- Author bio：
- Funds：
  
  Supported by the National Natural Science Foundation of China (No. 30700388) and Natural Science Foundation of Hubei Province, China (No. 2011CDB313)
- DOI：10.1007/s11655-014-1752-3
  CLC：
- Published：2015，
  
  Published Online：10 May 2014，
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Yang, Y., Li, Zh., Liu, H. et al. Inhibitory effect of tetramethylpyrazine preconditioning on overload training-induced myocardial apoptosis in rats., Chin. J. Integr. Med. 21, 423–430 (2015). https://doi.org/10.1007/s11655-014-1752-3

Yi Yang, Zhang-hua Li, Hua Liu, et al. Inhibitory effect of tetramethylpyrazine preconditioning on overload training-induced myocardial apoptosis in rats. [J]. Chinese Journal of Integrative Medicine 21(6):423-430(2015)
Yang, Y., Li, Zh., Liu, H. et al. Inhibitory effect of tetramethylpyrazine preconditioning on overload training-induced myocardial apoptosis in rats., Chin. J. Integr. Med. 21, 423–430 (2015). https://doi.org/10.1007/s11655-014-1752-3 DOI：

Yi Yang, Zhang-hua Li, Hua Liu, et al. Inhibitory effect of tetramethylpyrazine preconditioning on overload training-induced myocardial apoptosis in rats. [J]. Chinese Journal of Integrative Medicine 21(6):423-430(2015) DOI： 10.1007/s11655-014-1752-3.

摘要

To investigate the inhibitory effect of tetramethylpyrazine (Tet) preconditioning on overload training-induced myocardial apoptosis in rats

and to explore cardioprotective mechanisms of Tet preconditioning. A total of 25 male Sprague-Dawley rats were randomly divided into three groups

including the control group (n=5)

the overload training group (overload training for 8 weeks

n=10)

and the Tet preconditioning group (Tet preconditioning for 8 weeks before overload training

n=10). After 8 weeks

cardiac structure and myocardial apoptosis were analyzed by histology

transmission electron microscopy

and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay staining. The expressions of Bcl-2

Bax

Caspase-3

and Caspase-9 in myocardium were evaluated by immunohistochemical staining. Overload training caused swelling

disorder

partial rupture

and necrosis of myocardial focal necrotic fibers

as well as mitochondrial vacuolization

cristae rupturing

and blurring. In contrast

Tet preconditioning attenuated the swelling of myocardial fibers

decreased the amount of ruptured fibers

and inhibited mitochondrial vacuolization

resulting in clear cristae. Overload training significantly increased Bax expression and decreased Bcl-2/Bax ratio when compared with the control group (P<0.01). Conversely

Tet preconditioning significantly increased Bcl-2 expression and the Bcl-2/Bax ratio as compared with the overload training group (P<0.05). Overload training dramatically increased the expressions of Caspase-3 and Caspase-9 when compared with the control groupP<0.05). Following Tet preconditioning

the expression of Caspase-3 was significantly reduced compared with the overload training group (P<0.05)

while Caspase-9 expression showed a slight decline (P>0.05). Tet preconditioning increased the expression of Bcl-2 and reduced the expression of Caspase-3

thereby attenuating overload training-induced myocardial apoptosis

protecting against overload training-induced myocardial injury

and reducing damage to the myocardium due to overload training.

Abstract

To investigate the inhibitory effect of tetramethylpyrazine (Tet) preconditioning on overload training-induced myocardial apoptosis in rats

and to explore cardioprotective mechanisms of Tet preconditioning. A total of 25 male Sprague-Dawley rats were randomly divided into three groups

including the control group (n=5)

the overload training group (overload training for 8 weeks

n=10)

and the Tet preconditioning group (Tet preconditioning for 8 weeks before overload training

n=10). After 8 weeks

cardiac structure and myocardial apoptosis were analyzed by histology

transmission electron microscopy

and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay staining. The expressions of Bcl-2

Bax

Caspase-3

and Caspase-9 in myocardium were evaluated by immunohistochemical staining. Overload training caused swelling

disorder

partial rupture

and necrosis of myocardial focal necrotic fibers

as well as mitochondrial vacuolization

cristae rupturing

and blurring. In contrast

Tet preconditioning attenuated the swelling of myocardial fibers

decreased the amount of ruptured fibers

and inhibited mitochondrial vacuolization

resulting in clear cristae. Overload training significantly increased Bax expression and decreased Bcl-2/Bax ratio when compared with the control group (P<0.01). Conversely

the expression of Caspase-3 was significantly reduced compared with the overload training group (P<0.05)

while Caspase-9 expression showed a slight decline (P>0.05). Tet preconditioning increased the expression of Bcl-2 and reduced the expression of Caspase-3

thereby attenuating overload training-induced myocardial apoptosis

protecting against overload training-induced myocardial injury

and reducing damage to the myocardium due to overload training.

关键词

overload trainingtetramethylpyrazinepreconditioningmyocardial apoptosis

Keywords

overload trainingtetramethylpyrazinepreconditioningmyocardial apoptosis

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Intensive Care Unit, Guangdong Province Hospital of Chinese Medicine

Department of Anesthesiology, Xijing Hospital, Fourth Military Medical University

The First Affiliated Hospital of Xinxiang Medical College, Weihui

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