BACKGROUND:Cyclin A2 is a key regulator of cellcycle. Location and expression of cyclin A2 in neonatal mouse myocardium is not clear.
OBJECTIVE:To observe the location and expression of cyclin A2 in neonatal mouse cardiomyocytes and its relationship with the exit of cardiomyocytes from cellcycle.
METHODS:Neonatal mice were kil ed to take myocardial tissues at 0, 3, 7, 14 and 28 days after birth. Western blot were used to detect the expression of cyclin A2, proliferating cellnucleus antigen and Phospho-histone H3. Immunohistochemitry detection was used to detect the location of cyclin A2 and expression of proliferation cellnucleus antigen at different time after birth.
RESULTS AND CONCLUSION:Western blot showed the decrease of cyclin A2 after birth til disappeared at day 4 (P=0.001). Cyclin A2 located mainly in the nucleus after birth and exported to the cytoplasm at day 14, and basical y disappeared at day 28. Proliferating cellnucleus antigen showed gradual y decreased tendency after birth. Mitosis specific marker, Phospho-histone H3, exhibited a gradual decrease after birth, which was consistent with cyclin A2 in expression intensity.

With the rapid development of imaging and percutaneous coronary intervention, the application of contrast media has become more and more widespread, and contrast-associated AKI has become one of the most common causes of acute kidney injury. Contrast-associated AKI seriously threatens patients' health and brings greater economic burden to patients, so it is particularly important to prevent the contrast-associated AKI. Nicorandil is a common vasodilator drug in clinical practice, widely used in the treatment of angina pectoris, with the effects of anti-oxidative stress, anti-apoptosis, anti-inflammatory and vasodilation, and is considered to be effective in preventing contrast - associated AKI. However, there is still a lack of further research on the efficacy of nicorandil in preventing contrast-associated AKI.