Sudden Cardiac Death Natural Protection with Danshen Herb |Dr.Steve’s Bottom Line

Dr.Steve’s BOTTOM LINE: Tanshinone IIA one of the active ingredients  in the traditional Chinese herb  danshen (Salvia miltiorrhiza Bge), which is widely used in treatment of cardiovascular disorders, including high blood pressure.  Does it work? Prior studies show that this effect is due to vasodilation (relaxing blood vessels) via a complex mechanism called potassium channel blockade, which is something that some  conventional medicine anti-hypertensives and anti-arrhythmia drugs do as well. This study dug even deeper and found a possible scientific explanation for how this herb can lower sudden cardiac death at a micro-molecular level. Before you get too excited, these are early results from an animal study but it points to plausibility and possible human clinical trials using this herb for cardiac health.

Tanshinone IIA protects against sudden cardiac death induced by lethal arrhythmias via repression of microRNA-1.

Br J Pharmacol. 2009 Nov;158(5):1227-35

Authors: Shan H, Li X, Pan Z, Zhang L, Cai B, Zhang Y, Xu C, Chu W, Qiao G, Li B, Lu Y, Yang B

BACKGROUND AND PURPOSE: Tanshinone IIA is an active component of a traditional Chinese medicine based on Salvia miltiorrhiza, which reduces sudden cardiac death by suppressing ischaemic arrhythmias. However, the mechanisms underlying the anti-arrhythmic effects remain unclear. EXPERIMENTAL APPROACH: A model of myocardial infarction (MI) in rats by ligating the left anterior descending coronary artery was used. Tanshinone IIA or quinidine was given daily, before (7 days) and after (3 months) MI; cardiac electrical activity was monitored by ECG recording. Whole-cell patch-clamp techniques were used to measure the inward rectifying K(+) current (I(K1)) in rat isolated ventricular myocytes. Kir2.1 and serum response factor (SRF) levels were analysed by Western blot and microRNA-1 (miR-1) level was determined by real-time RT-PCR. KEY RESULTS: Tanshinone IIA decreased the incidence of arrhythmias induced by acute cardiac ischaemia and mortality in rats 3 months after MI. Tanshinone IIA restored the diminished I(K1) current density and Kir2.1 protein after MI in rat ventricular myocytes, while quinidine further inhibited I(K1)/Kir2.1. MiR-1 was up-regulated in MI, possibly due to the concomitant increase in SRF, a transcriptional activator of the miR-1 gene, accounting for decreased Kir2.1. Treatment with tanshinone IIA prevented increased SRF and hence increased miR-1 post-MI, whereas quinidine did not. CONCLUSIONS AND IMPLICATIONS: Down-regulation of miR-1 and consequent recovery of Kir2.1 may account partially for the efficacy of tanshinone IIA in suppressing ischaemic arrhythmias and cardiac mortality. These finding support the proposal that miR-1 could be a potential therapeutic target for the prevention of ischaemic arrhythmias.