Abstract
ObjectiveQishen Yiqi Drop Pill (QSYQ) has been recognized as a potential protective agent for various cardiovascular diseases. However, the effect of QSYQ in cardiac complications associated with diabetes is not clear currently. In this study, we investigate whether QSYQ could exert cardiac protective effects against high glucose‐induced injuries in cardiac H9c2 cells.MethodsH9c2 cells were exposed to 24 hours of high glucose in presence or absence of QSYQ and LY294002. Cell cytotoxicity, apoptosis, reactive oxygen species (ROS) generation, mitochondrial membrane potential and mitochondrial permeability transition pore (mPTP) opening were determined. Levels of bax, bcl‐2, p53, cleaved caspase‐3, PI3K and Akt were evaluated by Western blot.ResultsOur data indicated that QSYQ significantly increased the cell viability and decreased cytotoxicity. By analysing the apoptotic rate as well as the expression levels of cytoapoptosis‐related factors including cleaved caspase‐3, bax, bcl‐2, and p53, we found that QSYQ could remarkably suppress apoptosis of cardiomyoblasts caused by high glucose. In addition, it also showed that QSYQ reduced the generation of ROS. We further found that QSYQ treatment could inhibit the loss of mitochondrial membrane potential and mPTP opening. Moreover, Western blot analysis showed enhanced phosphorylation of PI3K/Akt. The specific inhibitor of PI3K, LY294002 not only inhibited QSYQ induced PI3K/Akt signalling pathway activation, but alleviated its protective effects.ConclusionsIn summary, these findings demonstrated that QSYQ effectively protected H9c2 cells against the series injuries due to high glucose at least partially by activating the PI3K/Akt signalling pathway.
Highlights
Diabetes mellitus (DM) is a worldwide public health problem
In 1972, Rubler found in four autopsy cases of diabetic patients that these patients had heart failure with‐ out obvious coronary artery or heart valve disease, congenital heart disease, hypertension or alcohol abuse, and he named this kind of heart disease as diabetes cardiomyopathy (DCM) for the first time.[7]
A number of studies have established the cellular model of DCM by using H9c2 cell line, which is generated from embryonic rat heart, to simulate DCM because of its near iden‐ tical pathological responses compared with that of primary cardio‐ myocytes.[17,18,19]
Summary
According to the latest data released by the International Diabetes Federation (IDF), the global diabetes patients rose to 415 million in 2015, accounting for about 8.3% of the total population of the adult population.[1,2] From 2012 to 2015, the number of deaths per year because of diabetes and its complications was as high as 1.5‐5.0 million.[3] Among the many complications of diabetes, cardiovascular disease (CVD) is still the leading cause of death in diabetes mellitus patients.[4] The Framingham heart study showed that the incidences of heart failure (HF) in men and women with diabetes were 2.4 and 5 times as high as that of healthy people, respectively.[5] the mortality of patients with heart failure complicated by diabetes increased significantly.[6] In addition, it suggests that diabetes is a risk factor for cardiovascular diseases such as coronary heart disease and hypertension, and the metabolic state of its own disorder has direct damage to the myocardium. A number of studies have established the cellular model of DCM by using H9c2 cell line, which is generated from embryonic rat heart, to simulate DCM because of its near iden‐ tical pathological responses compared with that of primary cardio‐ myocytes.[17,18,19] the aim of the current study is to verify whether QSYQ can protect cardiomyocytes against high glucose‐in‐ duced injuries and to explore the underlying mechanisms
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