International Heart Journal
Online ISSN : 1349-3299
Print ISSN : 1349-2365
ISSN-L : 1349-2365
Experimental Studies
Increased Bioavailable Berberine Protects Against Myocardial Ischemia Reperfusion Injury Through Attenuation of NFκB and JNK Signaling Pathways
Yang YuMing ZhangYali HuYali ZhaoFei TengXiaoyan LvJi LiYing ZhangGrant M. HatchLi Chen
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2018 Volume 59 Issue 6 Pages 1378-1388

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Abstract

Activation of Janus kinase (JNK) is involved in the pathogenesis of cardiac ischemia reperfusion injury. We previously demonstrated that oral treatment of rats with high doses of berberine (BBR) improved cardiac function in ischemia reperfusion injury. It is unknown if BBR modulates JNK activation. We developed a new formula, solid dispersion of BBR with sodium caprate (HGSD), which increases its bioavailability and membrane permeability. The present study examined if HGSD-mediated inhibition of JNK protects the heart from ischemia reperfusion injury.

The cardioprotective effect of HGSD was examined in rat hearts subjected to global 45 minutes ischemia followed by 30 minutes reperfusion. Hemodynamic parameters and troponin levels in the perfusate, and TNF-α, IL-6, JNK, and NFκB levels in the heart were determined. To further explore the cardioprotective mechanism of HGSD, H9c2 cells subjected to hypoxia/reoxygenation were incubated with serum containing HGSD in the absence or presence of an activator or inhibitor of JNK.

Pretreatment of rats with HGSD for 7 days significantly improved recovery of heart function in animals subjected to ischemia reperfusion injury compared to untreated controls. In addition, HGSD pretreatment inhibited cardiac production of TNF-α and IL-6, and attenuated ischemia reperfusion induced cardiac JNK activation and nuclear translocation of NFκB compared to untreated controls. In H9c2 cells subjected to hypoxia/reoxygenation, the presence of JNK activator diminished the release of TNF-α and IL-6 and the nuclear translocation of NFκB.

HGSD treatment protects the heart from ischemia reperfusion injury through attenuation of NFκB and JNK signaling pathways.

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© 2018 by the International Heart Journal Association
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