Int J Med Sci 2022; 19(1):65-73. doi:10.7150/ijms.64984 This issue

Review

Molecular-Signaling Pathways of Ginsenosides Rb in Myocardial Ischemia-Reperfusion Injury: A Mini Review

Fitri Fareez Ramli1,2, Adli Ali3,4, Nurul 'Izzah Ibrahim1,2✉

1. Department of Pharmacology, Faculty of Medicine, Universiti Kebangsaan Malaysia, 56000 Cheras, Kuala Lumpur, Malaysia.
2. Cardiovascular Health Research Group, Faculty of Medicine, Universiti Kebangsaan Malaysia, 56000 Cheras, Kuala Lumpur, Malaysia.
3. Department of Pediatrics, Faculty of Medicine, Universiti Kebangsaan Malaysia, 56000 Cheras, Kuala Lumpur, Malaysia.
4. Infection and Immunology Health and Advanced Medicine Cluster, Universiti Kebangsaan Malaysia, 56000 Cheras, Kuala Lumpur, Malaysia.

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Citation:
Ramli FF, Ali A, Ibrahim N'. Molecular-Signaling Pathways of Ginsenosides Rb in Myocardial Ischemia-Reperfusion Injury: A Mini Review. Int J Med Sci 2022; 19(1):65-73. doi:10.7150/ijms.64984. Available from https://www.medsci.org/v19p0065.htm

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Abstract

Graphic abstract

Reperfusion injury following myocardial ischemia remained a challenge for optimal treatment of myocardial infarction. Ginsenosides Rb (G-Rb), the primary components of ginsenoside, have been reported to exert cardioprotective effects via numerous mechanisms. G-Rb1 mediate cardioprotective effects via various signaling pathways, including mitochondrial apoptotic pathway, PI3K/Akt/mTOR, HIF-1α and GRF91, RhoA, p38α MAPK, and eNOS. G-Rb2 activates the SIRT-1 pathway, while G-Rb3 promotes both JNK-mediated NF-κB and PERK/Nrf2/HMOX1. Generally, ginsenosides Rb1, 2, and 3 modulates oxidative stress, inflammation, and apoptosis, contributing to the improvement of structural, functional and biochemical parameters. In conclusion, G-Rb, particularly G-Rb1, have vast potential as a supplement in attenuating reperfusion injury. Translation into a clinical trial is warranted to confirm the beneficial effects of G-Rb.

Keywords: molecular-signaling pathway, ginsenoside Rb1, ginsenoside Rb2, ginsenoside Rb3, myocardial ischemia-reperfusion injury