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.
Environ Toxicol Pharmacol. 2015 May;39(3):1132-8. doi: 10.1016/j.etap.2015.04.006. Epub 2015 Apr 13.
Epidemiological studies have revealed an association between sulfur dioxide (SO2) exposure and cardiovascular diseases. This study is designed to investigate the SO2 effect on the expression of ATP-sensitive K(+) (KATP) channel and L-type calcium (L-Ca(2+)) channel in rat hearts. The results show that the mRNA and protein levels of the KATP channel subunits Kir6.2 and SUR2A of rat hearts in SO2 groups were higher than those in control group. SO2 at 14mg/m(3) significantly decreased the expression of the L-Ca(2+) channel subunits Cav1.2 and Cav1.3. This suggests that SO2 can activate the KATP channels by up-regulating the expression of Kir6.2 and SUR2A, while it inhibits the L-Ca(2+) channels by down-regulating the expression of Cav1.2 and Cav1.3 in rat hearts. The molecular mechanism of SO2-induced negative inotropic effect might be linked to the expression changes of these subunits, which may contribute to the pathogenesis of SO2-associated cardiovascular diseases.
流行病学研究表明，二氧化硫（SO2）暴露与心血管疾病之间存在关联。本研究旨在探讨 SO2 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，SO2 组大鼠心脏的 KATP 通道亚基 Kir6.2 和 SUR2A 的 mRNA 和蛋白水平均高于对照组。14mg/m（3）的 SO2 显著降低了 L-Ca（2+）通道亚基 Cav1.2 和 Cav1.3 的表达。这表明 SO2 可以通过上调 Kir6.2 和 SUR2A 的表达来激活 KATP 通道，同时通过下调 Cav1.2 和 Cav1.3 的表达来抑制大鼠心脏中的 L-Ca（2+）通道。SO2 引起的负性肌力作用的分子机制可能与这些亚基的表达变化有关，这可能有助于 SO2 相关心血管疾病的发病机制。
