OR WAIT null SECS
A recent animal study found that administration of pyrroloquinoline quinone (PQQ) from Nascent Health Sciences reduced the risk of chronic heart failure.
A recent animal study1, conducted both in vivo on Sprague Dawley rats and in vitro on neonatal rat left ventricle myocytes (NRVM), found that administration of pyrroloquinoline quinone (PQQ) from Nascent Health Sciences (Iselin, NJ) reduced the risk of chronic heart failure. The study was conducted by the Department of Cardiology at an affiliated hospital of Nantong University (Nantong, China). In the study, 42 rats were subjected to transaortic constriction (TAC) and 20 were subjected to a sham surgery. After the procedures, 30 rats were randomized to receive PQQ intragastrically at low, medium, or high doses (0.4, 2, 10 mg/kg) daily for 12 weeks. The remaining rats were administered 2 ml of saline (placebo) daily, for 12 weeks.
Results showed that TAC caused significant ventricular and myocyte hypertrophy in rats, as evidenced by heart sizes, and increased heart weight/body weight ratios. Compared to rats who received sham surgeries, PQQ attenuated these changes at 2 and 10 mg/kg doses. PQQ also reversed left ventricular contractile function and fractional shortening percentage at all doses, while 2 and 10 mg/kg doses significantly reduced left end-systolic internal diameter.
At 2 and 10 mg/kg, PQQ also had a greater effect on mRNA expression levels of heart failure markers, compared to placebo. While 2 and 10 mg/kg doses were both found to have therapeutic effects, 10 mg/kg of PQQ showed no concentration-dependent effects, meaning 2 mg/kg of PQQ was in fact the best therapeutic dose. When left ventricle heart tissue from the rats was observed under an electron microscope, results showed that TAC increased the severity of mitochondrial morphology, however PQQ treatment after TAC protected the morphology of mitochondria. PQQ also protected heart mitochondrial function by regulating mitochondrial biogenesis changes.
In vitro, NVRMs were pretreated with 1, 10, and 100 µM PQQ for 24 h. After pretreatment, 200 nm angiotensin II was added to the NRVMs, with or without PQQ, for 48 hours in order to establish a model of cardiac pressure overload. Results showed that PQQ regulated mitochondrial biogenesis changes in vitro in addition to in vivo, and attenuated the increase of reactive oxygen species (ROS) levels.
“For the first time ever, the positive benefits of the powerful antioxidant PQQ on myocardial mitochondrial dysfunction and chronic heart failure have been demonstrated,” said Thomas Schrier, vice president of sales at Nascent Health Sciences, in a statement. “The researchers at Nantong University were specifically looking for treatment options to target mitochondrial function in the heart and have now found conclusive evidence that PQQ’s ability to stimulate mitochondrial biogenesis can prevent cardiac damage and promote heart health.”