Key result
MLC901 reduces acute myocardial infarct size by ~50% in mice with ischemia-reperfusion injury.
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Demonstrates acute and long-term cardioprotection by MLC901 in mice, indicating reduced infarct size, decreased fibrosis, and improved cardiac recovery.
MLC901, a traditional Chinese medicine containing a cocktail of active molecules, both reduces cerebral infarction and improves recovery in patients with ischemic stroke. The aim of this study was to evaluate the acute and long-term benefits of MLC901 in ischemic and reperfused mouse hearts. Ex vivo, under physiological conditions, MLC901 did not show any modification in heart rate and contraction amplitude. However, upon an ischemic insult, MLC901 administration during reperfusion, improved coronary flow in perfused hearts. In vivo, MLC901 (4 µg/kg) intravenous injection 5 minutes before reperfusion provided a decrease in both infarct size (49.8%) and apoptosis (49.9%) after 1 hour of reperfusion. Akt and ERK1/2 survival pathways were significantly activated in the myocardium of those mice. In the 4-month clinical follow-up upon an additional continuous per os administration, MLC901 treatment decreased cardiac injury as revealed by a 45%-decrease in cTnI plasmatic concentrations and an improved cardiac performance assessed by echocardiography. A histological analysis revealed a 64%-decreased residual scar fibrosis and a 44%-increased vascular density in the infarct region. This paper demonstrates that MLC901 treatment was able to provide acute and long-term cardioprotective effects in a murine model of myocardial ischemia-reperfusion injury in vivo.
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Vincent et al. (2017) studied Myocardial ischemia-reperfusion injury. MLC901 was evaluated on Infarct size, apoptosis, cardiac injury (cTnI), residual scar fibrosis, and vascular density (49.8% decrease in infarct size, 49.9% decrease in apoptosis, 45% decrease in cTnI, 64% decrease in scar fibrosis). MLC901 reduced myocardial infarct size by 49.8% acutely and decreased residual scar fibrosis by 64% at 4 months in mice with ischemia-reperfusion injury.
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