Abstract
Objective: Determine the role of uncoupling protein 2 (UCP2) in the myocardial apoptosis of diabetic mellitus（DM）. Methods: DM animal models were induced by streptozotocinon (STZ) on UCP2 knock-out mice (UCP2KO) and wild-type mice (WT), which were reared for 7 and 28 days after successful modeling, respectively. The expressions of relative protein for myocardial apoptosis, pro-caspase-9, were investigated using western blot. However, the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) was used to explain apoptosis at the DNA level. Results: Image analysis showed that the expression of pro-caspase-9 protein levels increased slightly in UCP-/- + DM-7-day group comparing with DM-7-day group (P > 0.05). The expression of pro-caspase-9 protein levels increased significantly (P < 0.05）in UCP-/- + DM-28-day group comparing with DM-28-day group. TUNEL analysis indicated that UCP2 reduced the number of apoptotic myocytes in the DM-28-day group by 70% in comparison to DM-7-day group by 30% (P < 0.05). Conclusion UCP2 may be one of the most important factors that contribute to the myocardial apoptosis of DM.
Highlights
An inner mitochondrial protein known as uncoupling protein 2 (UCP2) is a member of the uncoupling protein family and belongs to the inner mitochondrial membrane anion-carrier superfamily
Hyperglycemia is considered to be the primary cause of most chronic diabetic complications, such as cardiovascular pathological changes, diabetic retinopathy, diabetic nephropathy, diabetic foot, etc., which occurs via the deregulation of β-cell insulin secretion and the development of peripheral tissue insulin resistance
Therein, they observed that there was a close relationship between myocardial apoptosis and the occurrence or development of diabetic cardiomyopathy
Summary
An inner mitochondrial protein known as uncoupling protein 2 (UCP2) is a member of the uncoupling protein family and belongs to the inner mitochondrial membrane anion-carrier superfamily. UCP2 can be detected in the heart [1], brain, lung, spleen, kidney, liver, and adipose tissue. UCP2 is a regulator of reactive oxygen species during electron transport in the mitochondrial inner membrane, plays an active role in the prevention of atherosclerosis [2], is one of the etiologies of type 2 diabetes [3], participates in inflammation [4], and regulates cell apoptosis [5]and aging [6]. The purpose of this study was to investigate the relationship between UCP2 and the myocardial apoptosis of diabetic mellitus, demonstrate the important role of UCP2 in diabetic cardiomyopathy (DC), and provide additional theoretical foundation for DC therapy
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