Ginsenoside RK3 Prevents Hypoxia-Reoxygenation Induced Apoptosis in H9c2 Cardiomyocytes via AKT and MAPK Pathway | Zendy

Jing Sun | Zendy; Guibo Sun | Zendy; Xiangbao Meng | Zendy; Hongwei Wang | Zendy; Min Wang | Zendy; Meng Qin | Zendy; Bo Ma | Zendy; Yun Luo | Zendy; Yingli Yu | Zendy; Rongchang Chen | Zendy; Qidi Ai | Zendy; Xiaobo Sun | Zendy

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Ginsenoside RK3 Prevents Hypoxia-Reoxygenation Induced Apoptosis in H9c2 Cardiomyocytes via AKT and MAPK Pathway

Author(s) -

Jing Sun,

Guibo Sun,

Xiangbao Meng,

Hongwei Wang,

Min Wang,

Meng Qin,

Bo Ma,

Yun Luo,

Yingli Yu,

Rongchang Chen,

Qidi Ai,

Xiaobo Sun

Publication year - 2013

Publication title -

evidence-based complementary and alternative medicine

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.552

H-Index - 90

eISSN - 1741-4288

pISSN - 1741-427X

DOI - 10.1155/2013/690190

Subject(s) - panax notoginseng , protein kinase b , apoptosis , tunel assay , hypoxia (environmental) , pharmacology , cardioprotection , mapk/erk pathway , pi3k/akt/mtor pathway , medicine , viability assay , myocardial infarction , ginsenoside , reperfusion injury , chemistry , ginseng , ischemia , signal transduction , biochemistry , pathology , alternative medicine , organic chemistry , oxygen

Reperfusion therapy is widely utilized for acute myocardial infarction (AMI), but further injury induced by rapidly initiating reperfusion of the heart is often encountered in clinical practice. Ginsenoside RK3 (RK3) is reportedly present in the processed Radix notoginseng that is often used as a major ingredient of the compound preparation for ischemic heart diseases. This study aimed to investigate the possible protective effect of RK3 against hypoxia-reoxygenation (H/R) induced H9c2 cardiomyocytes damage and its underlying mechanisms. Our results showed that RK3 pretreatment caused increased cell viability and decreased levels of LDH leakage compared with the H/R group. Moreover, RK3 pretreatment inhibited cell apoptosis, as evidenced by decreased caspase-3 activity, TUNEL-positive cells, and Bax expression, as well as increased Bcl-2 level. Further mechanism investigation revealed that RK3 prevented H9c2 cardiomyocytes injury and apoptosis induced by H/R via AKT/Nrf-2/HO-1 and MAPK pathways. These observations indicate that RK3 has the potential to exert cardioprotective effects against H/R injury, which might be of great importance to clinical efficacy for AMI treatment.

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