Propofol attenuates H2O2-induced oxidative stress and apoptosis via the mitochondria- and ER-medicated pathways in neonatal rat cardiomyocytes

被引:39
作者
Liu, Xue-Ru [1 ]
Cao, Lu [1 ]
Li, Tao [2 ]
Chen, Lin-Lin [2 ]
Yu, Yi-Yan [2 ]
Huang, Wen-Jun [2 ]
Liu, Li [1 ]
Tan, Xiao-Qiu [2 ]
机构
[1] Southwest Med Univ, Dept Anesthesiol, Affiliated Hosp, Luzhou, Peoples R China
[2] Southwest Med Univ, Collaborat Innovat Ctr Prevent & Treatment Cardio, Key Lab Med Electrophysiol, Minist Educ,Inst Cardiovasc Res, Luzhou, Peoples R China
关键词
Propofol; Oxidative stress; Apoptosis; Cardiomyocyte; ENDOPLASMIC-RETICULUM STRESS; ISCHEMIA-REPERFUSION; MYOCARDIAL-ISCHEMIA; UP-REGULATION; CELLS; ACTIVATION; PROTECTS; DISEASE; INJURY; HEART;
D O I
10.1007/s10495-017-1349-3
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Previous studies have shown that propofol, an intravenous anesthetic commonly used in clinical practice, protects the myocardium from injury. Mitochondria- and endoplasmic reticulum (ER)-mediated oxidative stress and apoptosis are two important signaling pathways involved in myocardial injury and protection. The present study aimed to test the hypothesis that propofol could exert a cardio-protective effect via the above two pathways. Cultured neonatal rat cardiomyocytes were treated with culture medium (control group), H2O2 at 500 mu M (H2O2 group), propofol at 50 mu M (propofol group), and H2O2 plus propofol (H2O2 + propofol group), respectively. The oxidative stress, mitochondrial membrane potential (Delta I<spacing diaeresis>m) and apoptosis of the cardiomyocytes were evaluated by a series of assays including ELISA, flow cytometry, immunofluorescence microscopy and Western blotting. Propofol significantly suppressed the H2O2-induced elevations in the activities of caspases 3, 8, 9 and 12, the ratio of Bax/Bcl-2, and cell apoptosis. Propofol also inhibited the H2O2-induced reactive oxygen species (ROS) generation, lactic dehydrogenase (LDH) release and mitochondrial transmembrane potential (Delta I<spacing diaeresis>m) depolarization, and restored the H2O2-induced reductions of glutathione (GSH) and superoxide dismutase (SOD). In addition, propofol decreased the expressions of glucose-regulated protein 78 kDa (Grp78) and inositol-requiring enzyme 1 alpha (IRE1 alpha), two important signaling molecules in the ER-mediated apoptosis pathway. Propofol protects cardiomyocytes from H2O2-induced injury by inhibiting the mitochondria- and ER-mediated apoptosis signaling pathways.
引用
收藏
页码:639 / 646
页数:8
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