Abstract
Our previous study has demonstrated that 6-Gingerol (6-G) could alleviate myocardial ischemia/reperfusion injury (MIRI). However, the molecular mechanism underlying the process of myocardial ischemia/reperfusion (I/R) injury alleviation by 6-G remains unelucidated. The objective of the present study is to further investigate the potential mechanism for 6-G to alleviate MIRI in rats. Thirty-two Sprague-Dawley rats were randomly divided into four groups: the Sham group, the I/R group, the 6-G + I/R group, and the LY294002 (LY) + 6-G + I/R group. For the rats in each of the groups, data were collected for cardiogram, cardiac function, area of myocardial infarction, myocardial pathology, myocardial enzyme, marker of inflammatory response, and PI3K/Akt signaling pathway. We found that the pretreatment of 6-G with 6 mg/kg could shrink the ST section of cardiogram, improve the cardiac function, reduce the area of myocardial infarction and the degree of cardiac pathological injury, lower the level of myocardial enzyme, and inhibit the inflammatory response. In addition, our results also indicated that 6-G could upregulate the expression of PI3K and p-Akt and that LY294002, a blocking agent of PI3K/Akt signaling pathway, could nullify the protecting role of 6-G. Our experimental results showed that 6-G could inhibit I/R-induced inflammatory response through the activation of the PI3K/Akt signaling pathway.
Highlights
Acute myocardial infarction (AMI) is the main cause for the incidence and death of coronary heart disease (CHD) in the world [1]
We investigated the role of 6-G in myocardial protection by inhibition of inflammatory response and further examined whether 6-G participated in the Phosphoinositide-3 kinase (PI3K)/Aktdependent mechanism
TNFa, IL-6, IL-1β, NLRP3, and caspase-1 were provided by Abcam (Cambridge, UK). 2,3,5-triphenyltetrazolium chloride (TTC), BCA protein quantification kit, and the second antibody were purchased from Beyotime (Changsha, China)
Summary
Acute myocardial infarction (AMI) is the main cause for the incidence and death of coronary heart disease (CHD) in the world [1]. In the same time of saving lives, reperfusion can lead to the death of myocardial cell and induce abnormal cardiac function, i.e., myocardial ischemia/reperfusion injury (MIRI) [3, 4]. It has been found that inflammatory response, oxidative induction, and apoptosis all play core roles in the incidence and development of MIRI [5]. Inflammation participates in the pathophysiological process of a variety of cardiovascular diseases, such as myocardial infarction (MI), cardiac hypoxia/reoxygenation (H/R) injury, MIRI, and ischemic heart diseases [6]. Increasing evidences confirmed that inflammation plays a crucial role in MIRI, and it has been proven to be one of the markers for ischemia/reperfusion (I/R) injury. I/R could induce local or systemic massive release of inflammatory
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