Imperatorin protects H9c2 cardiomyoblasts cells from hypoxia/reoxygenation-induced injury through activation of ERK signaling pathway

• Published in: Saudi pharmaceutical journal Vol. 25; no. 4; pp. 615 - 619
• Main Authors: Liao, Bihong, Chen, Ruimian, Lin, Feng, Mai, Aihuan, Chen, Jie, Li, Huimin, Dong, Shaohong, Xu, Zhenglei
• Format: Journal Article
• Language: English
• Published: Saudi Arabia Elsevier B.V 01.05.2017; Elsevier
• Subjects: Apoptosis; ERK signaling pathway; H9c2 cardiomyoblasts; Hypoxia/reoxygenation; Imperatorin; Original; Imperatorin; H9c2 cardiomyoblasts; ERK signaling pathway; Hypoxia/reoxygenation; Apoptosis
• ISSN: 1319-0164; 2213-7475
• DOI: 10.1016/j.jsps.2017.04.033

Imperatorin is a compound found in plants and has been widely used in Chinese medicine for many years. It has many pharmacological effects, including the recently reported anti-apoptotic function, however, the mechanism largely remains unclear. This study is aimed to elucidate the mechanism of Imperatorin’s anti-apoptotic function. A model of hypoxia and reoxygenation (H/R) treated h9c2 cardiomyoblasts was successfully constructed. The cells were treated with H/R condition, and followed by adding Imperatorin alone, Imperatorin with ERK inhibitor and/or ERK inhibitor alone, to examine the cell viability by Cell Counting Kit-8 assay, cell apoptosis rate by flow cytometry, and ERK expression by Western-blot under different conditions. The results showed that imperatorin exerted protective effect on h9c2 cells from H/R injure. It was also found that it not only increased cell viability but also reduced the apoptotic rate for H/R treated h9c2 cells. The experiments also demonstrated that imperatorin could upregulate the expression levels of both ERK1 and ERK2, which is a key step in ERK signaling pathway activation. These findings provided evidence that imperatorin could increase the cell viability and lower apoptotic rate in H/R treated h9c2 cells, and could also enhance the expression of ERK1/ERK2, demonstrating imperatorin’s protective effect on H/R injured h9c2 cells through ERK signaling pathway.