焦亚硫酸钠对大鼠心脏中KATP和L-Ca2+通道表达的分子机制
The molecular mechanisms of sodium metabisulfite on the expression of K ATP and L-Ca2+ channels in rat hearts.
作者信息
Zhang Quanxi, Bai Yunlong, Yang Zhenhua, Tian Jingjing, Meng Ziqiang
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
Regul Toxicol Pharmacol. 2015 Aug;72(3):440-6. doi: 10.1016/j.yrtph.2015.05.021. Epub 2015 May 23.
Sodium metabisulfite (SMB) is used as an antioxidant and antimicrobial agent in a variety of drugs and foods. However, there are few reported studies about its side effects. This study is to investigate the SMB effects on the expression of ATP-sensitive K(+) (KATP) and L-type calcium (L-Ca(2+)) channels in rat hearts. The results show that the mRNA and protein levels of the KATP channel subunits Kir6.2 and SUR2A were increased by SMB; on the contrary, SMB at 520 mg/kg significantly decreased the expression of the L-Ca(2+) channel subunits Cav1.2 and Cav1.3. This suggests that SMB can activate the expression of KATP channel by increasing the mRNA and protein levels of Kir6.2 and SUR2A, while it inhibits the expression of L-Ca(2+) channels by decreasing the mRNA and protein levels of Cav1.2 and Cav1.3 in rat hearts. Therefore, the molecular mechanism of the SMB effect on rat hearts might be related to the increased expression of KATP channels and the decreased expression of L-Ca(2+) channels.
焦亚硫酸钠（SMB）在多种药物和食品中用作抗氧化剂和抗菌剂。然而，关于其副作用的报道研究较少。本研究旨在探讨SMB对大鼠心脏中ATP敏感性钾（KATP）通道和L型钙（L-Ca(2+)）通道表达的影响。结果表明，SMB可使KATP通道亚基Kir6.2和SUR2A的mRNA和蛋白水平升高；相反，520mg/kg的SMB显著降低了L-Ca(2+)通道亚基Cav1.2和Cav1.3的表达。这表明SMB可通过增加Kir6.2和SUR2A的mRNA和蛋白水平来激活KATP通道的表达，同时通过降低大鼠心脏中Cav1.2和Cav1.3的mRNA和蛋白水平来抑制L-Ca(2+)通道的表达。因此，SMB对大鼠心脏作用的分子机制可能与KATP通道表达增加和L-Ca(2+)通道表达降低有关。
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