Thaliporphine, an alkaloid from Neolitsea konishii, exerts antioxidant, anti-inflammatory, and anti-apoptotic responses in guinea pig during cardiovascular collapse in inflammatory disease

被引:5
作者
Ku, Hui-Chun [1 ]
Lee, Shih-Yi [1 ,2 ,3 ]
Lee, Shoei-Sheng [4 ]
Su, Ming-Jai [1 ]
机构
[1] Natl Taiwan Univ, Inst Pharmacol, Coll Med, 1,Sec 1,Jen Ai Rd, Taipei 10051, Taiwan
[2] Mackay Mem Hosp, Div Pulm & Crit Care Med, Taipei, Taiwan
[3] Mackay Jr Coll Med Nursing & Management, Taipei, Taiwan
[4] Natl Taiwan Univ, Sch Pharm, Taipei, Taiwan
关键词
Thaliporphine; Cardiovascular; Reactive oxygen species; QT interval; Apoptosis; Inflammatory; NITRIC-OXIDE; CARDIOMYOCYTE APOPTOSIS; SIGNALING PATHWAY; OXIDATIVE STRESS; SEPSIS; INSULIN; PEROXYNITRITE; SUPEROXIDE; INHIBITION; MYOCYTES;
D O I
10.1016/j.jff.2016.07.002
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Excessive production of inflammatory cytokines and reactive oxygen species causes circulatory abnormalities leading to insufficient oxygen supply, which results in organ ischaemia and failure. Cardiovascular collapse enhances the risk of death in inflammatory disease. The present study examined the protective effects of thaliporphine, an alkaloid derived from Neolitsea konishii, during cardiovascular collapse in inflammatory disease, which was induced by LPS injection following coronary artery occlusion in guinea pig. Thaliporphine alleviated oxidative stress by preserving SOD activity and accompanied with the alleviation in inflammatory response, was observed to decrease NO, TNF-alpha secretion and hyperglycaemic response. In addition, thaliporphine inhibited cell death-related pathways activation, as seen by reduced JNK phosphorylation, bax expression, and capase-3 activity, leading to the reduction of myocardial infarct size and prolongation of QT interval in heart. The findings indicate that thaliporphine induces antioxidant, anti-inflammatory, and anti-apoptotic effects and may be developed for the prevention of inflammatory disease with cardiovascular system disorder. (C) 2016 Published by Elsevier Ltd.
引用
收藏
页码:57 / 64
页数:8
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