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. 2018 Oct 25;9:1138. doi: 10.3389/fphar.2018.01138

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Copyright © 2018 Ma, Yu, Chen, Li, Ihsan, Tong, Huang and Gao.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The cardiac protective mechanism of sweroside on aconitine-exposed H9c2 cells. Aconitine upregulated the function of Na⁺ channels to cause increase of intracellular Na⁺ ions leading to intracellular Ca²⁺ overload, which induced excess ROS production. The large accumulation of ROS triggered cellular autophagy/apoptosis, even death. Sweroside reversed effectively aconitine-induced cell damage.