Quercetin Attenuates Ethanol-Induced Iron Uptake and Myocardial Injury by Regulating the Angiotensin II-L-Type Calcium Channel.

摘要: SCOPE Increased iron deposition in the myocardium alcoholics may lead to increased risk of cardiac dysfunction. Quercetin has been demonstrated quench production intracellular free iron-induced -OH, but effect quercetin ethanol-induced damage remains unclear. This study aims explore whether attenuates uptake and myocardial injury by regulating angiotensin II-L-type voltage-dependent Ca2+ channel (Ang II-LTCC). METHODS AND RESULTS Adult male C57BL/6J mice are isocalorically pair-fed either a regular or ethanol-containing Lieber De Carli liquid diets supplemented with (100 mg kg-1  bw) desferrioxamine mesylate (DFO, 100 bw) for 15 weeks. alleviated histopathological changes, creatine kinase isoenzyme release, Ang II secretion, ROS generation, total iron, labile level. Ethanol exposure intervention fails regulate traditional transporters except LTCC. LTCC is upregulated ethanol inhibited quercetin. In H9C2 cell, (100 mm) and/or (1 μm) concomitant disorders oxidative stress. partially normalized (50 μm), nifedipine (LTCC inhibitor, losartan receptor antagonist, μm). CONCLUSION Alcohol-induced associated excessive NTBI mediated II-LTCC activation which be against cardiotoxicity.