科研之友
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摘要
Aim To explore the role of cotranscriptional activator p300 in regulating the electrical remodeling of atrial myocytes in aging mouse, which resulted in atrial fibrillation. Methods The left atrial appendage tissues of 5 , 13 and 18monthold C57BL/6 mice were collected respectively. Western blot was used to detect the protein expression levels of p300, L type calcium channel (Cavl. 2) and aging related protein p53/p21. Acute enzymatic hydrolysis was used to isolate single atrial myocytes, and the wholecell patchclamp technique was used to detect the Ltype calcium current (ICa,L) and action potential duration (APD) of atrial myocytes. The susceptibility of atrial fibrillation was detected by electrophysiological examination. Results Compared with 5monthold mice, the protein expression of p300, p53 and p21 in the left atrial appendage of mice increased in 13monthold and 18monthold C57B L / 6 mice (P < 0.05), while the expression of Cav 1.2 decreased. The peak current of / c a, L in atrial myocytes of 18monthold C57BL/6 mice was significantly reduced, and the APD was shortened. Treatment of p300 inhibitorcurcumin (5 0, 100 mg ? kg-1 ? d-1) significantly reduced the inducible rate of atrial fibrillation through increasing ICa,L and prolonging APD of atrial myocytes in elderly mice (P < 0. 05). Conclusion p300 may participate in the aginginduced electrical remodeling of atrial myocytes by regulating ICa,L ? 2021 Publication Centre of Anhui Medical University.
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