Host: The Japanese Pharmacological Society, The Japanese Society of Clinical Pharmacology
Name : WCP2018 (18th World Congress of Basic and Clinical Pharmacology)
Location : Kyoto
Date : July 01, 2018 - July 06, 2018
Background: Aconitine(ACO) as the main active component in Aconitum plants has analgesia and anti-inflammation effect, while aconitine also has highly toxicity in heart. However, the mechanisms of poison are not clear yet. Aconite Decoction(WTT) is a traditional Chinese herbal prescription for treating RA in China for thousands of years. Aconitum carmichaelii (Fuzi,) and Herbaceous peony(Shaoyao,) both are the key herbs in WTT, Paeoniflorin(PF) is the main chemical ingredient in Herbaceous peony which has good efficacy on RA with less adverse effects. Besides, PF also protects heart against injury by anti-platelet agglutinating, antioxidant, vasodilator effect and other effects. So, in this study, we focus on investigate the possibility of PF combined with aconitine for reducing its cardiotoxicity.
Methods: We study the research from several directions including cell proliferation, apoptosis, ion channels and energy metabolism. We chose H9c2 cells as experimental subject. MTT test, Western Blot and Real-time PCR were used to determine cell proliferation, apoptosis (the level of Bcl-2, Bax, p53 and Capase-3), ion channels (SCN5A, RyR2 and Cx43 mRNA) respectively. Finally, according to LDH, SOD and MDA kit instructions, extracellular LDH and intracellular SOD and MDA all were measured.
Results:Cell proliferation in ACO+PF group was significantly increased compared with ACO groups; the ratio with Bcl-2 and Bax and the level of p53 was upregulated by PF, while the level of Capase-3 was lightly reduced. The expression of SCN5A mRNA was suppressed in ACO group and significantly increased in ACO+PF groups, the expression of RyR2 mRNA is an opposite respond, as well as Cx43, PF has inhibited the change of expression of Cx43 mRNA induced by ACO. Compared with ACO group, extracellular LDH and intracellular MDA was highly decreased, intracellular SOD was regulated.
Conclusions:
The data above may demonstrate that the cardiotoxicity of ACO in H9c2 cells was significantly decreased by PF.
