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Notoginsenoside R Prevents H9c2 Cardiomyocytes Apoptosis Against Hypoxia/reoxygenation the ERs/PI3K/Akt Pathway

Overview
Journal RSC Adv
Specialty Chemistry
Date 2022 May 11
PMID 35539324
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Abstract

Notoginsenoside R (NGR) is separate from Panax notoginsenosides (PNS), and plays a role similar to phytoestrogen in preventing and treating cardiovascular diseases. However, the protective mechanism of NGR in the myocardial ischemia/reperfusion injury the estrogen receptor (ER) pathway remains unclear, which hinder its application. This study aimed to study the preventive mechanisms of NGR in the apoptosis of H9c2 cardiomyocytes after hypoxia/reoxygenation (H/R). NGR did not affect the expression of ERα and ERβ proteins in normal H9c2 cardiomyocytes. However, NGR could upregulate the ERα and G protein-coupled receptor 30 (GPR30) proteins in H9c2 cardiomyocytes after H/R without affecting ERβ levels. Moreover, it significantly affected the expression levels of PI3K and its downstream apoptosis proteins such as Bcl-2 Associated X Protein (Bax), B cell lymphoma/lewkmia-2 (Bcl-2), caspase-3, and so forth. Whereas, after adding the PI3K protein antagonist, the modulatory expression levels of PI3K and its downstream apoptosis proteins were remarkably abolished. After adding ERα and GPR30 antagonists, NGR had no significant effect on the expression of PI3K and its downstream Akt protein in the model group. The data of flow cytometry showed that after adding the ERα, GPR30 and PI3K antagonists, the apoptotic rate of cardiomyocytes had no significant changes compared with the model group. This study demonstrated that NGR protected H9c2 cardiomyocytes from the injury after H/R by affecting ERα and GPR30 to regulate the expression levels of PI3K and its downstream apoptosis proteins.

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References
1.
Perrone G, Capri O, Galoppi P, Patacchioli F, Bevilacqua E, De Stefano M . Menopausal symptoms after the discontinuation of long-term hormone replacement therapy in women under 60: a 3-year follow-up. Gynecol Obstet Invest. 2013; 76(1):38-43. DOI: 10.1159/000351104. View

2.
Manson J, Chlebowski R, Stefanick M, Aragaki A, Rossouw J, Prentice R . Menopausal hormone therapy and health outcomes during the intervention and extended poststopping phases of the Women's Health Initiative randomized trials. JAMA. 2013; 310(13):1353-68. PMC: 3963523. DOI: 10.1001/jama.2013.278040. View

3.
Meng X, Sun G, Wang M, Sun J, Qin M, Sun X . P90RSK and Nrf2 Activation via MEK1/2-ERK1/2 Pathways Mediated by Notoginsenoside R2 to Prevent 6-Hydroxydopamine-Induced Apoptotic Death in SH-SY5Y Cells. Evid Based Complement Alternat Med. 2013; 2013:971712. PMC: 3789498. DOI: 10.1155/2013/971712. View

4.
Su P, Du S, Li H, Li Z, Xin W, Zhang W . Notoginsenoside R1 inhibits oxidized low-density lipoprotein induced inflammatory cytokines production in human endothelial EA.hy926 cells. Eur J Pharmacol. 2015; 770:9-15. DOI: 10.1016/j.ejphar.2015.11.040. View

5.
Zhong L, Zhou X, Liu Y, Wang Y, Ma F, Guo B . Estrogen receptor α mediates the effects of notoginsenoside R1 on endotoxin-induced inflammatory and apoptotic responses in H9c2 cardiomyocytes. Mol Med Rep. 2015; 12(1):119-26. PMC: 4438911. DOI: 10.3892/mmr.2015.3394. View