Cardiovascular diseases (CVD) are a range of situations that affects heart and blood vessels including coronary artery disease, heart failure, hypertensive heart disease, cardiomyopathy, peripheral artery disease and etc [98, 99]. In 2008, 30% of all worldwide death was credited to CVD. It is valued that by 2030, above 23 million people will die from CVD each year [100]. Pharmacological interventions in people with CVD can lead to occur potential side effects. So, numerous natural products have been assessed for pharmacological therapy [77]. Shu L et al, have shown TXR has cardioprotective effects in in vivo and in vitro models via decreasing levels of TNF-?, IL-10 and some apoptosis markers such as Bax and caspase 3 as well as activating PI3K/Akt signaling pathway and markedly reducing myocardial infarct size [101].
In another study on rats, TRX alleviated myocardial ischemia-reperfusion (I/R) damage by inhibition of miR?146a?5p, apoptotic factors such as Bcl-2 as well as attenuated I/R damage?induced insufficiency of hemodynamic factors of heart, CK, LDH and proinflammatory cytokines [102].
TRX shows beneficial roles as cardioprotective agent on arrhythmias induced by I/R that significantly decreased the number of premature ventricular complexes and duration and frequency of ventricular fibrillation as well as markedly decreased myocardial proinflammatory cytokine levels of TNF-? and IL-1? after I/R compared to untreated group [103]. Another investigation suggested TRX had inhibitory effect on GSK-3? via increasing its phosphorylation form, thus attenuated apoptotic index after I/R in diabetic myocardium of rats [70]. Badalzadeh et al have demonstrated TRX has protective effects on diabetes-induced vascular injuries in rat aorta and reduced vascular histopathological injuries in compared to untreated diabetic rats.
They also shown TXR elevated the activity of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPX) and reduced the levels of MDA (the major product of lipid peroxidation) [68]. Mitochondrial dysfunction is an important role in cardiac disease inventing from the metabolic syndrome (MS). In high fat, high fructose diet (HFFD) -induced mouse model of MS, decreasing respiratory chain complex activity mtDNA content and mitochondrial biogenesis as well as increasing in oxidative stress factors and reactive oxygen species (ROS) generation occurred which TRX administration reversed these effects and showed beneficial roles in mouse model of MS [104]
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