Cardioprotective effect of notoginsenoside R1 in a rabbit lung remote ischemic postconditioning model via activation of the TGF‑β1/TAK1 signaling pathway

  • Authors:
    • Zhi‑Ru Ge
    • Mao‑Chun Xu
    • Yu Huang
    • Chen‑Jun Zhang
    • Je Lin
    • Chang‑Wu Ruan
  • View Affiliations

  • Published online on: April 4, 2016     https://doi.org/10.3892/etm.2016.3222
  • Pages: 2341-2348
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Abstract

Pharmacological postconditioning using cardioprotective agents is able to reduce myocardial infarct size. Notoginsenoside R1 (NG‑R1), a phytoestrogen isolated from Panax notoginseng saponins (PNS), is considered to have anti‑oxidative and anti‑apoptotic properties. However, its cardioprotective properties and underlying mechanisms remain largely unknown. The aim of the present study was to determine the cardioprotective and anti‑apoptotic effects of NG‑R1 in an ischemia‑reperfusion (IR)‑induced myocardial injury rabbit model. A total of 45 Japanese big‑ear rabbits were equally randomized to three groups: Control group, remote ischemic postconditioning (RIP) group and NG‑R1 intervention group. At the endpoint of the experiment, the animals were sacrificed to remove myocardial tissues for the detection of transforming growth factor (TGF)‑β1‑TGF‑β activated kinase 1 (TAK1) pathway‑related proteins by immunohistochemistry and western blot analysis, the activities of caspase‑3, ‑8 and ‑9 in myocardial cells by fluorometric assay, and the apoptosis of myocardial cells by terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labeling. Right and left lung tissues were stained with hematoxylin and eosin (H&E) to observe the severity of injury. NG‑R1 treatment reduced the activity of superoxide dismutase, increased the content of malondialdehyde, reduced the activities of caspase‑3, ‑8 and ‑9, and inhibited the apoptosis of myocardial cells in rabbits undergoing RIP. In addition, the expression of TGF‑β1‑TAK1 signaling pathway‑related proteins was downregulated following NG‑R1 intervention. H&E staining of bilateral lung tissues showed that cell morphology was generally intact without significant alveolar congestion, and there was no significant difference among the three groups. These results indicate that NG‑R1 protects the heart against IR injury, possibly by inhibiting the activation of the TGF‑β1‑TAK1 signaling pathway and attenuating apoptotic stress in the myocardium.
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June-2016
Volume 11 Issue 6

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Ge ZR, Xu MC, Huang Y, Zhang CJ, Lin J and Ruan CW: Cardioprotective effect of notoginsenoside R1 in a rabbit lung remote ischemic postconditioning model via activation of the TGF‑β1/TAK1 signaling pathway. Exp Ther Med 11: 2341-2348, 2016
APA
Ge, Z., Xu, M., Huang, Y., Zhang, C., Lin, J., & Ruan, C. (2016). Cardioprotective effect of notoginsenoside R1 in a rabbit lung remote ischemic postconditioning model via activation of the TGF‑β1/TAK1 signaling pathway. Experimental and Therapeutic Medicine, 11, 2341-2348. https://doi.org/10.3892/etm.2016.3222
MLA
Ge, Z., Xu, M., Huang, Y., Zhang, C., Lin, J., Ruan, C."Cardioprotective effect of notoginsenoside R1 in a rabbit lung remote ischemic postconditioning model via activation of the TGF‑β1/TAK1 signaling pathway". Experimental and Therapeutic Medicine 11.6 (2016): 2341-2348.
Chicago
Ge, Z., Xu, M., Huang, Y., Zhang, C., Lin, J., Ruan, C."Cardioprotective effect of notoginsenoside R1 in a rabbit lung remote ischemic postconditioning model via activation of the TGF‑β1/TAK1 signaling pathway". Experimental and Therapeutic Medicine 11, no. 6 (2016): 2341-2348. https://doi.org/10.3892/etm.2016.3222