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Pretreatment with low-dose gadolinium chloride attenuates myocardial ischemia/reperfusion injury in rats
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Pretreatment with low-dose gadolinium chloride attenuates myocardial ischemia/reperfusion injury in rats
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Pretreatment with low-dose gadolinium chloride attenuates myocardial ischemia/reperfusion injury in rats
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Journal Article
Pretreatment with low-dose gadolinium chloride attenuates myocardial ischemia/reperfusion injury in rats
2016
Overview
Aim： We have shown that low-dose gadolinium chloride （GdCI3） abolishes arachidonic acid （AA）-induced increase of cytoplasmic Ca2＋, which is known to play a crucial role in myocardial ischemia/reperfusion （I/R） injury. The present study sought to determine whether low-dose GdCI3 pretreatment protected rat myocardium against I/R injury in vitro and in vivo. Methods： Cultured neonatal rat ventricular myocytes （NRVMs） were treated with GdCI3 or nifedipine, followed by exposure to anoxia/ reoxygenation （A/R）. Cell apoptosis was detected; the levels of related signaling molecules were assessed. SD rats were intravenously injected with GdCI3 or nifedipine. Thirty min after the administration the rats were subjected to LAD coronary artery ligation followed by reperfusion. Infarction size, the release of serum myocardial injury markers and AA were measured; cell apoptosis and related molecules were assessed. Results： In A/R-treated NRVMs, pretreatment with GdCl3 （2.5, 5, 10 pmoVL） dose-dependently inhibited caspase-3 activation, death receptor-related molecules DR5/Fas/FADD/caspase-8 expression, cytochrome c release, AA release and sustained cytoplasmic Ca2＋ increases induced by exogenous AA. In I/R-treated rats, pre-administration of GdCl3 （10 mg/kg） significantly reduced the infarct size, and the serum levels of CK-MB, cardiac troponin-I, LDH and AA. Pre-administration of GdCl3 also significantly decreased the number of apoptotic cells, caspase-3 activity, death receptor-related molecules （DR5/Fas/FADD） expression and cytochrome c release in heart tissues. The positive control drug nifedipine produced comparable cardioprotective effects in vitro and in vivo. Conclusion： Pretreatment with low-dose GdCl3 significantly attenuates I/R-induced myocardial apoptosis in rats by suppressing activation of both death receptor and mitochondria-mediated pathways.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Arachidonic Acid - pharmacology
/ Biomedical and Life Sciences
/ Gadolinium - administration & dosage
/ Gadolinium - therapeutic use
/ Male
/ Mitochondria, Heart - drug effects
/ Mitochondria, Heart - metabolism
/ Myocardial Reperfusion Injury - drug therapy
/ Myocardial Reperfusion Injury - pathology
/ Myocytes, Cardiac - drug effects
/ Myocytes, Cardiac - pathology
/ Original
/ Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism
/ Signal Transduction - drug effects
/ Vaccine
/ 低剂量
/ 心肌损伤
/ 心肌细胞凋亡
/ 新生大鼠
/ 氯化钆
/ 缺血/再灌注损伤
/ 预处理
