Abstract
ObjectiveWe investigated the protective effect of tetramethylpyrazine (TMP) on injury related to acute myocardial ischemia (AMI) induced by isoproterenol (ISO).Materials and methodsRats were randomly assigned to five groups: control, ISO, ISO + propranolol (10 mg/kg), ISO + TMP (10 mg/kg) and ISO + TMP (20 mg/kg). The rats in the three ISO + groups were pretreated with propranolol or TMP, while the rats in the control and ISO groups were pretreated with an equal volume of saline. Afterwards, the rats in the four administration groups were subcutaneously injected with ISO for two consecutive days. The levels of creatine kinase (CK), lactate dehydrogenase (LDH), superoxide dismutase (SOD), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1β in the serum were measured using ELISA. The expressions of B-cell lymphoma-associated X-2 (Bax-2), B-cell lymphoma-2 (Bcl-2), phosphoinositide-3-kinase (PI3K), protein kinase B (Akt), glycogen synthase kinase 3β (GSK-3β), MDA5 and SOD1 were determined using western blotting assay. The phosphorylation of PI3K, Akt and GSK-3β were also determined using western blotting assay. The left ventricles of the rats were extracted and stained using hematoxylin and eosin (H&E). The ST segment was recorded using electrocardiograms (ECGs).ResultsAdministration of TMP (10, 20 mg/kg) reduced the levels of MDA and CK and the activities of SOD and LDH in the serum. Pretreatment with TMP significantly reduced the levels of pro-inflammatory cytokines, including IL-1β, IL-6 and TNF-α. Treatment with TMP also improved the histopathological alteration and decreased the ST elevation. Furthermore, TMP ameliorated the expressions of Cu, SOD1, MDA5, Bax-2, Bcl-2, p-PI3K, p-Akt and p-GSK-3β in ISO-induced rats.ConclusionsTetramethylpyrazine protected against injury due to AMI by regulating the PI3K/Akt /GSK-3β signaling pathway.
Highlights
The leading cause of morbidity in the Western world is acute myocardial ischemia (AMI), which is caused by an imbalance between the blood supply to the heart and the demand of the myocardium [1, 2]
Tetramethylpyrazine protected against injury due to AMI by regulating the PI3K/Akt /glycogen synthase kinase 3β (GSK-3β) signaling pathway
We further investigated the cardioprotective effect of TMP and assessed whether the PI3K/Akt/GSK-3β signal pathway was involved in the cardioprotective effect of TMP
Summary
The leading cause of morbidity in the Western world is acute myocardial ischemia (AMI), which is caused by an imbalance between the blood supply to the heart and the demand of the myocardium [1, 2]. The primary features of AMI are hypoxia, cell ischemia and inflammation. Obstruction of the blood flow to the heart contributes to the ischemia of myocardial cells, which may contribute to the apoptotic process [3,4,5]. Isoproterenol (ISO), a β-adrenergic agonist, is known to induce AMI due to autoxidation-related free radical production [7]. ISO-induced AMI increases the levels of cardiac enzymes and oxidative stress, and results in abnormal electrocardiograph and cardiac functions [8]
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