%0 Journal Article
%T Metabolomic profiles of myocardial ischemia under treatment with salvianolic acid B
%A Yonghai Lu
%A Yue Zheng
%A Xinru Liu
%A Xu Liang
%A Saiming Ngai
%A Tiejun Li
%A Weidong Zhang
%J Chinese Medicine
%D 2012
%I BioMed Central
%R 10.1186/1749-8546-7-6
%X Five conventional Western medicines (isosorbide dinitrate, verapamil, propranolol, captopril and trimethazine) with different mechanisms for treating cardiovascular diseases were selected as positive references to compare with SA-B in changing of the metabolomic profiles in MI rats under treatment. Potential mechanisms of SA-B were further investigated in H9C2 cell line.The metabolomic profiles between SA-B- and propranolol-treated MI rats were similar, since there was a big overlap between the two groups in the PLS-DA score plot. Finally, it was demonstrated that SA-B exhibited a protective effect on MI mainly by decreasing the concentration of cyclic adenosine monophosphate (cAMP) and Ca2+ and inhibiting protein kinase A (PKA).SA-B and propanolol exhibited similar metabolomic profiles, indicating that the two drugs might have a similar mechanism.Myocardial ischemia (MI) is characterized by ischemia in the heart muscle. It is the most common cause of death, and a major reason for hospital admissions [1]. In MI, ¦Â-adrenoceptor is generally activated. Noradrenaline binds to ¦Â-adrenoceptor to activate GS protein. Then, adenylate cyclase (AC) is activated by GS protein, which makes adenosine triphosphate (ATP) to be cyclic adenosine monophosphate (cAMP). cAMP in turn activates the cAMP-dependent protein kinase A (PKA). This kinase phosphorylates several proteins related to excitation-contraction coupling, such as L-type Ca2+ channel and phospholamban. The phosphorylation of L-type Ca2+ channel causes the Ca2+ influx, leading to stronger muscle contraction. The phosphorylation of phospholamban accelerates Ca2+ uptake into the sarcoplasmic reticulum, increasing the rate and extent of muscle relaxation [2,3].¦Â-adrenergic blockers such as propranolol [4] could inhibit the activation of ¦Â-adrenoceptor and decrease the concentration levels of cAMP, PKA and Ca2+, leading to slow heart rate, decreased myocardial contractility, reduced cardiac output, and decreased myocardial o
%U http://www.cmjournal.org/content/7/1/6