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亚硫酸钠对体内和体外大鼠主动脉 BK(Ca)、K(ATP)和 L-Ca(2+)通道表达的影响。

Effects of sodium metabisulfite on the expression of BK(Ca), K(ATP), and L-Ca(2+) channels in rat aortas in vivo and in vitro.

机构信息

Institute of Environmental Medicine and Toxicology, Institute of Environmental Science, Shanxi University, Taiyuan 030006, China.

Institute of Environmental Medicine and Toxicology, Institute of Environmental Science, Shanxi University, Taiyuan 030006, China.

出版信息

J Hazard Mater. 2015 Mar 2;284:151-62. doi: 10.1016/j.jhazmat.2014.10.053. Epub 2014 Nov 11.

Abstract

Sodium metabisulfite (SMB) is most commonly used as the preservative in many food preparations and drugs. So far, few studies about its negative effects were reported. The purpose of this study was to investigate the effect of SMB on the expression of big-conductance Ca(2+)-activated K(+) (BKCa), ATP-sensitive K(+) (KATP), and L-type calcium (L-Ca(2+)) channels in rat aorta in vivo and in vitro. The results showed that the mRNA and protein levels of the BKCa channel subunits α and β1 of aorta in rats were increased by SMB in vivo and in vitro. Similarly, the expression of the KATP channel subunits Kir6.1, Kir6.2, and SUR2B were increased by SMB. However, SMB at the highest concentration significantly decreased the expression of the L-Ca(2+) channel subunits Cav1.2 and Cav1.3. These results suggest that SMB can activate BKCa and KATP channels by increasing the expression of α, β1, and Kir6.1, Kir6.2, SUR2B respectively, while also inhibit L-Ca(2+) channels by decreasing the expression of Cav1.2 and Cav1.3 of aorta in rats. The molecular mechanism of SMB-induced vasorelaxant effect might be related to the expression changes of BKCa, KATP, and L-Ca(2+) channels subunits. Further work is needed to determine the relative contribution of each channel in SMB-mediated vasorelaxant effect.

摘要

亚硫酸钠(SMB)最常用于许多食品制剂和药物的防腐剂。到目前为止,关于其负面影响的研究报道很少。本研究旨在探讨 SMB 对大鼠主动脉体内和体外大电导钙激活钾(BKCa)、ATP 敏感性钾(KATP)和 L 型钙(L-Ca(2+))通道表达的影响。结果表明,SMB 体内和体外均可增加大鼠主动脉 BKCa 通道亚基 α 和 β1 的 mRNA 和蛋白水平。同样,KATP 通道亚基 Kir6.1、Kir6.2 和 SUR2B 的表达也增加。然而,最高浓度的 SMB 显著降低了 L-Ca(2+)通道亚基 Cav1.2 和 Cav1.3 的表达。这些结果表明,SMB 可以通过增加 α、β1 和 Kir6.1、Kir6.2、SUR2B 的表达分别激活 BKCa 和 KATP 通道,同时通过降低 Cav1.2 和 Cav1.3 的表达来抑制大鼠主动脉中的 L-Ca(2+)通道。SMB 诱导血管舒张作用的分子机制可能与 BKCa、KATP 和 L-Ca(2+)通道亚基的表达变化有关。需要进一步的工作来确定每个通道在 SMB 介导的血管舒张作用中的相对贡献。

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