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Article

Ginsenoside Rb1 protects cardiomyocytes from oxygen‑glucose deprivation injuries by targeting microRNA‑21

  • Authors:
    • Chuang Yang
    • Bo Li
    • Yongsheng Liu
    • Yue Xing
  • View Affiliations / Copyright

    Affiliations: Department of Cardiology, Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China
  • Pages: 3709-3716
    |
    Published online on: March 1, 2019
       https://doi.org/10.3892/etm.2019.7330
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Abstract

Ginsenoside Rb1 (GS‑Rb1) is one of the most important active pharmacological extracts of the traditional Chinese medicine, ginseng, and there is extensive evidence of its cardioprotective properties. However, the microRNA (miR) targets of GS‑Rb1 and the underlying mechanisms of GS‑Rb1 and miR‑21 in the progression of cardiomyocyte apoptosis have not been clearly elucidated. The aim of the current study was to investigate the impact of miR‑21 and its target gene, programmed cell death protein 4 (PDCD4), on the protective effect of GS‑Rb1 in cardiomyocytes injured by oxygen‑glucose deprivation (OGD). The miR‑21 expression levels were downregulated, and the percentage of the apoptotic cells and reactive oxygen species (ROS) was increased in OGD‑cultured neonatal rat cardiomyocytes; however, the effects were reversed by GS‑Rb1 treatment. It was demonstrated that GS‑Rb1 could reduce intracellular ROS content, and the expression of cytochrome C and the pro‑apoptosis protein, apoptosis regulator B‑cell lymphoma associated X (Bax) protein while increasing the expression of the anti‑apoptosis protein, apoptosis regulator Bcl‑2. The target gene, PDCD4, was significantly upregulated in the OGD group; however, the expression of PDCD4 was inhibited by GS‑Rb1 treatment. Furthermore, miR‑21 inhibitor transfection reduced GS‑Rb1‑induced miR‑21 upregulation compared with the OGD+GS‑Rb1 group, indicating that the miR‑21 was involved in the anti‑apoptotic effect of GS‑Rb1 in cardiomyocytes. The results of the current study highlighted that GS‑Rb1 could target miR‑21 and its target gene, PDCD4, to protect OGD‑injured cardiomyocytes. The results of the current study may provide a novel insight for the treatment of myocardial infarction with Traditional Chinese Medicines, involving miRs as targets.
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Copy and paste a formatted citation
Spandidos Publications style
Yang C, Li B, Liu Y and Xing Y: Ginsenoside Rb1 protects cardiomyocytes from oxygen‑glucose deprivation injuries by targeting microRNA‑21. Exp Ther Med 17: 3709-3716, 2019.
APA
Yang, C., Li, B., Liu, Y., & Xing, Y. (2019). Ginsenoside Rb1 protects cardiomyocytes from oxygen‑glucose deprivation injuries by targeting microRNA‑21. Experimental and Therapeutic Medicine, 17, 3709-3716. https://doi.org/10.3892/etm.2019.7330
MLA
Yang, C., Li, B., Liu, Y., Xing, Y."Ginsenoside Rb1 protects cardiomyocytes from oxygen‑glucose deprivation injuries by targeting microRNA‑21". Experimental and Therapeutic Medicine 17.5 (2019): 3709-3716.
Chicago
Yang, C., Li, B., Liu, Y., Xing, Y."Ginsenoside Rb1 protects cardiomyocytes from oxygen‑glucose deprivation injuries by targeting microRNA‑21". Experimental and Therapeutic Medicine 17, no. 5 (2019): 3709-3716. https://doi.org/10.3892/etm.2019.7330
Copy and paste a formatted citation
x
Spandidos Publications style
Yang C, Li B, Liu Y and Xing Y: Ginsenoside Rb1 protects cardiomyocytes from oxygen‑glucose deprivation injuries by targeting microRNA‑21. Exp Ther Med 17: 3709-3716, 2019.
APA
Yang, C., Li, B., Liu, Y., & Xing, Y. (2019). Ginsenoside Rb1 protects cardiomyocytes from oxygen‑glucose deprivation injuries by targeting microRNA‑21. Experimental and Therapeutic Medicine, 17, 3709-3716. https://doi.org/10.3892/etm.2019.7330
MLA
Yang, C., Li, B., Liu, Y., Xing, Y."Ginsenoside Rb1 protects cardiomyocytes from oxygen‑glucose deprivation injuries by targeting microRNA‑21". Experimental and Therapeutic Medicine 17.5 (2019): 3709-3716.
Chicago
Yang, C., Li, B., Liu, Y., Xing, Y."Ginsenoside Rb1 protects cardiomyocytes from oxygen‑glucose deprivation injuries by targeting microRNA‑21". Experimental and Therapeutic Medicine 17, no. 5 (2019): 3709-3716. https://doi.org/10.3892/etm.2019.7330
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