Kobophenol A Inhibits Sodium Nitroprusside-induced Cardiac H9c2 Cell Death through Suppressing Activation of JNK and Preserving Mitochondrial Anti-apoptotic Bcl-2 and Mcl-1

Sung Ryul Lee; Jong Hwan Kwak; Su Jin Noh; Julius Ryan Pronto; Kyung Soo Ko; Byoung Doo Rhee; Zhelong Xu; Nari Kim; Jin Han

doi:10.1248/cpb.c13-00995

This article has now been updated. Please use the final version.

Kobophenol A Inhibits Sodium Nitroprusside-induced Cardiac H9c2 Cell Death through Suppressing Activation of JNK and Preserving Mitochondrial Anti-apoptotic Bcl-2 and Mcl-1

Sung Ryul Lee, Jong Hwan Kwak, Su Jin Noh, Julius Ryan Pronto, Kyung Soo Ko, Byoung Doo Rhee, Zhelong Xu, Nari Kim, Jin Han

Author information

Sung Ryul Lee
National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Department of Health Sciences and Technology, Inje University
Jong Hwan Kwak
School of Pharmacy, Sungkyunkwan University
Su Jin Noh
National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Department of Health Sciences and Technology, Inje University
Julius Ryan Pronto
National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Department of Health Sciences and Technology, Inje University
Kyung Soo Ko
National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Department of Health Sciences and Technology, Inje University
Byoung Doo Rhee
National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Department of Health Sciences and Technology, Inje University
Zhelong Xu
Department of Physiology & Pathophysiology, Tianjin, Medical University
Nari Kim
National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Department of Health Sciences and Technology, Inje University
Jin Han
National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Department of Health Sciences and Technology, Inje University

Keywords: Caragana sinica, Kobophenol A, Sodium nitroprusside, JNK, Bcl-2, Mcl-1

JOURNAL FREE ACCESS Advance online publication

Article ID: c13-00995

DOI https://doi.org/10.1248/cpb.c13-00995

The final version of this article is now available: Vol. 62 (2014), No. 7 pp. 713-718

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Abstract

Sodium nitroprusside (SNP) releases nitric oxide (NO), a powerful vasodilator, and thus widely used in intensive care unit for treating hypertension emergency. However, cardiac toxicity after SNP administration is a clinical problem. For finding a natural compound that suppressing SNP-induced cardiac toxicity, we tested the protective potential of kobophenol A (Kob A), purified from the root of Caragana sinica, against the toxic effects of SNP. The severe cardiac H9c2 cell death was induced by SNP (2 mM) treatment. Kob A ameliorated SNP-induced cardiac H9c2 cell death, and this protective effect of Kob A may be related to the inhibition of JNK and p38 MAP kinase activation following SNP administration. In addition, the downregulation of cellular Bcl-2 and Mcl-1 levels by SNP exposure was strongly abrogated in the presence of Kob A. These biological properties of Kob A might provide insights into developing new cardioprotectant against SNP-induced cardiac cell death.

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