Abstract
Objective. This study aimed to evaluate the protective effect of kaempferol against myocardial ischemia/reperfusion (I/R) injury in rats. Method. Left ventricular developed pressure (LVDP) and its maximum up/down rate (±dp/dt max) were recorded as myocardial function. Infarct size was detected with 2,3,5-triphenyltetrazolium chloride staining. Cardiomyocyte apoptosis was determined using terminal deoxynucleotidyl nick-end labeling (TUNEL). The levels of creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione/glutathione disulfide (GSH/GSSG) ratio, and tumor necrosis factor-alpha (TNF-α) were determined using enzyme linked immunosorbent assay (ELISA). Moreover, total glycogen synthase kinase-3β (GSK-3β), phospho-GSK-3β (P-GSK-3β), precaspase-3, cleaved caspase-3, and cytoplasm cytochrome C were assayed using Western blot analysis. Results. Pretreatment with kaempferol significantly improved the recovery of LVDP and ±dp/dt max, as well as increased the levels of SOD and P-GSK-3β and GSH/GSSG ratio. However, the pretreatment reduced myocardial infarct size and TUNEL-positive cell rate, as well as decreased the levels of cleaved caspase-3, cytoplasm cytochrome C, CK, LDH, MDA, and TNF-α. Conclusion. These results suggested that kaempferol provides cardioprotection via antioxidant activity and inhibition of GSK-3β activity in rats with I/R.
Highlights
Nowadays, cardiovascular diseases are responsible for the majority of elderly mortality [1]; the most important presentation of cardiovascular disease is ischemia
We investigated the effects of kaempferol on cardiac function, myocardial Infarct Size (IS), cardiomyocyte apoptosis, inflammation factor, and myocardial enzyme in the isolated rat heart model of I/R
We provided evidence that kaempferol improves the recovery of cardiac function, reduces intracellular oxidation status and myocardial IS, and inhibits myocardial apoptosis induced by I/R
Summary
Cardiovascular diseases are responsible for the majority of elderly mortality [1]; the most important presentation of cardiovascular disease is ischemia. A long period of ischemia leads to myocardial injury. Restoring blood supply to the ischemic myocardium can reduce myocardial injury. Reperfusion can aggravate myocardial damage through ischemia-reperfusion (I/R) injury [2]. Excessive reactive oxygen species (ROS), calcium overload, inflammatory reaction, and other factors can lead to cellular necrosis, apoptosis, and organ dysfunction in severe cases [3]. Prevention of I/R is important to alleviate ischemic heart disease [4]
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