Effects of N-n-butyl haloperidol iodide on the rat myocardial sarcoplasmic reticulum Ca2+–ATPase during ischemia/reperfusion

Luteolin Exerts Cardioprotective Effects through Improving Sarcoplasmic Reticulum Ca2+-ATPase Activity in Rats during Ischemia/Reperfusion In Vivo

“…However, this finding was not consistent with the results reported in other in vitro studies [ 1 , 2 ]. Although Zhang et al [ 12 ] found no change in SERCA2a expression levels in response to short-term myocardial I/R, the evidence was insufficient to reach a conclusion because the longest reperfusion period in their study was only 120 min, while the half-life of SERCA2a is about 5 days. We confirmed that there were no alterations in SERCA2a expression levels in vivo during I/R because the reperfusion duration of our study was prolonged to 7 days.…”

“…Moreover, this study found that increased reperfusion duration led to a further decrease in SERCA2a activity, which was restored by prolonged myocardial I/R duration. Zhang et al [ 12 ] reported that SERCA2a activity decreased after ischemia for 30–60 min followed by reperfusion for 0–120 min. They indicated that SERCA2a activities in the I/R groups observed for 30/0 min, 30/30 min, and 30/120 min all decreased by more than 55%, and the extent of this decrease was similar among these groups ( P > 0.05).…”

“…The chest was opened via left thoracotomy through the fifth intercostal space to reveal the beating apex of the heart. After pericardiotomy, a silk suture was placed under the left anterior descending coronary artery (LAD) between the left auricle and pulmonary arterial cone, and the ends of the suture were threaded through a small plastic tube and fixed with an artery clamp to form a reversible occlusion of the LAD [ 12 , 15 ]. The sham group only underwent thoracotomy and pericardiotomy.…”

“…However, the in vivo cardioprotective effects of luteolin and its actions on SERCA2a during I/R injury remain largely unknown. Moreover, Zhang et al [ 12 ] found that SERCA2a activity decreased during I/R injury in vivo, independent of SERCA2a protein level modulation during short-term myocardial I/R injury. However, the reperfusion time used in their model may have been too short to detect relevant changes in protein expression because the longest reperfusion duration in their study was only 120 min, although the half-life of SERCA2a is about 5 days.…”

Myocardial ischemia/reperfusion injury: Mechanisms of injury and implications for management (Review)

“…Unfolded proteins in ERS induce myocardial injury, which further induces ERS, thereby affecting the metabolic state of cardiomyocytes and causing greater injury ( 86 ). During MIRI, ERS is increased and inhibition of ERS has been shown to attenuate MIRI ( 88-90 ). However, it has also been reported that not all ERS is harmful.…”