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

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Summary

Introduction

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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