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CQ10 Improved Cardiac Function in Rats with Acute Myocardial Ischemia-Reperfusion Injury.
CQ10 Increased Direct Energy Supply in Rats with Acute Myocardial Ischemia-Reperfusion Injury.
As previously reported, CQ10 plays a key role in the mitochondrial respiratory chain by preventing oxidative stress injury to the mitochondrial membrane [29, 30].
In our study, Atg5, beclin-1, and the ratio of LC-3II to LC3-I, which represent autophagy activity, are increased after acute ischemia-reperfusion injury with CQ10 preconditioning.
In our study, apoptosis protein levels are reduced by CQ10 preconditioning.
In all, antioxidative function, energy survival, and autophagy activation are the major causes of infarct size reduction and cardiac function improvement after acute ischemia-reperfusion injury with CQ10 preconditioning.
In order to sufficiently evaluate whether CQ10 preconditioning reduces or only delays the detrimental effect of ischemiare-perfusion injury, a research designed for different doses of CQ10 and a long of outcome after ischemia-reperfusion injury is needed.
In summary, we have established that CQ10 preconditioning regulates the balance of antioxidants and oxidants, enhances autophagy levels and activity, reduces myocardial apoptosis, and improves cardiac function in rats with acute ischemia-reperfusion injury.
Caption: Figure 1: CQ10 enhanced autophagy in rats with acute myocardial ischemia-reperfusion injury.
Caption: Figure 2: CQ10 decreased p62 protein expression (as grayscale ratio of p62 to [beta]-actin) in rats with acute myocardial ischemia-reperfusion injury.
(b and c) CQ10 decreases apoptosis-associated protein expression of p53 and caspase-3.
(b) DAPI/Bak/Bax immunofluorescence staining in different time of AMI/R + CQ10 group.
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