Cardioprotective Effect of Licochalcone D against Myocardial Ischemia/Reperfusion Injury in Langendorff-Perfused Rat Hearts

PLoS One

Qiu-sheng Zheng¹  Chang-gui Li²  Hong Zhao²  Peng-long Wang²  Xuan Yuan³  Shi-han Liu³  Hai-tao Niu³  Jie Lu³ 

[1] Binzhou Medical College, Yantai, 264000, Shandong, China;Key Laboratory of Xinjiang Endemic Phytomedicine Resources, Ministry of Education, School of Pharmacy, Shihezi University, Shihezi, 832002, Xinjiang, China;The Affiliated Hospital of Qingdao University, Qingdao, 266003, Shandong, China

关键词: Heart;    Apoptosis;    Inflammation;    Nitric oxide;    Reperfusion;    MAPK signaling cascades;    Ischemia;    Oxidative stress;   

DOI  :  10.1371/journal.pone.0128375

学科分类：医学（综合）

来源: Public Library of Science

【 摘 要 】

Flavonoids are important components of ‘functional foods’, with beneficial effects on cardiovascular function. The present study was designed to investigate whether licochalcone D (LD) could be a cardioprotective agent in ischemia/reperfusion (I/R) injury and to shed light on its possible mechanism. Compared with the I/R group, LD treatment enhanced myocardial function (increased LVDP, dp/dtmax, dp/dtmin, HR and CR) and suppressed cardiac injury (decreased LDH, CK and myocardial infarct size). Moreover, LD treatment reversed the I/R-induced cleavage of caspase-3 and PARP, resulting in a significant decrease in proinflammatory factors and an increase in antioxidant capacity in I/R myocardial tissue. The mechanisms underlying the antiapoptosis, antiinflammation and antioxidant effects were related to the activation of the AKT pathway and to the blockage of the NF-κB/p65 and p38 MAPK pathways in the I/R-injured heart. Additionally, LD treatment markedly activated endothelial nitric oxide synthase (eNOS) and reduced nitric oxide (NO) production. The findings indicated that LD had real cardioprotective potential and provided support for the use of LD in myocardial I/R injury.

【 授权许可】

CC BY