2. Academic Validation
  3. Cardioprotective effects of Notoginsenoside R1 against ischemia/reperfusion injuries by regulating oxidative stress- and endoplasmic reticulum stress- related signaling pathways

Cardioprotective effects of Notoginsenoside R1 against ischemia/reperfusion injuries by regulating oxidative stress- and endoplasmic reticulum stress- related signaling pathways

  • Sci Rep. 2016 Feb 18;6:21730. doi: 10.1038/srep21730.
Yingli Yu 1 2 3,  Guibo Sun 1 2 3,  Yun Luo 1 2 3,  Min Wang 1 2 3,  Rongchang Chen 1 2 3,  Jingyi Zhang 1 2 3,  Qidi Ai 1 2 3,  Na Xing 4,  Xiaobo Sun 1 2 3
Affiliations

Affiliations

  • 1 Beijing Key Laboratory of Innovative Drug Discovery of Traditional Chinese Medicine (Natural Medicine) and Translational Medicine, Institute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, 100193, China.
  • 2 Key Laboratory of Bioactive Substances and Resource Utilization of Chinese Herbal Medicine, Ministry of Education, China.
  • 3 Zhongguancun Open Laboratory of the Research and Development of Natural Medicine and Health Products, China.
  • 4 Key Laboratory of Chinese Materia Medica, Heilongjiang University of Chinese Medicine, Harbin, 150040, China.
PMID: 26888485 DOI: 10.1038/srep21730
Abstract

Background: Recent reports suggested the involvement of oxidative stress- and endoplasmic reticulum stress (ERS)-associated pathways in the progression of ischemia/reperfusion (I/R) injury. Notoginsenoside R1 (NGR1) is a novel saponin isolated from P. notoginseng, which has a history of prevention and treatment of cardiovascular diseases.

Objective: We aimed to examine the cardioprotective effects of NGR1 on I/R-induced heart dysfunction ex vivo and in vitro.

Methods: H9c2 cadiomyocytes were incubated with NGR1 for 24 h and exposed to hypoxia/reoxygenation. Isolated rat hearts were perfused by NGR1 for 15 min and then subjected to global ischemia/reperfusion. Hemodynamic parameters were monitored as left ventricular systolic pressure (LVSP), heart rate, and maximal rate of increase and decrease of left ventricular pressure (± dP/dt max/min).

Results: NGR1 pretreatment prevents cell Apoptosis and delays the onset of ERS by decreasing the protein expression levels of ERS-responsive proteins GRP78, P-PERK, ATF6, IRE, and inhibiting the expression of pro-apoptosis proteins CHOP, Caspase-12, and P-JNK. Besides, NGR1 scavenges free radical, and increases the activity of antioxidase. NGR1 inhibits Tunicamycin-induced cell death and cardiac dysfunction.

Conclusion: We elucidated the significant cardioprotective effects of NGR1 against I/R injuries, and demonstrated the involvement of oxidative stress and ERS in the protective effects of NGR1.

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