Ginsenoside Rb1 reduces oxidative stress and improves cardiac dysfunction induced by mechanical trauma in rats

AIM To explore whether Ginsenoside Rb1 (GRb1) improves cardiac dysfunction induced by mechanical trauma (MT) in rats and the underlying mechanisms. METHODS Anesthetized rats were subjected to 200 revolutions at a rate of 30 rpm in Noble-Collip drum to induce a nonlethal mechanical trauma and the rats were randomized to receive vehicle or GRb1. An in vitro study was performed on cultured cardiomyocytes subjected to sham-traumatic serum (SS), traumatic serum (TS), traumatic serum and Ginsenoside Rb1(TS+GRb1) or traumatic serum and TEMPOL (TS+TEMPOL). RESULTS Cardiac superoxide dismutase SOD (P<0.01) levels dropped and malondialdehyde MDA (P<0.01) production was significantly elevated at 2hr after MT, which led to diminished cardiac function at 24 hr after MT, as evidenced by decreased LVDP and±dP/dt_max (P<0.01). GRb1 treatment significantly reduced ROS production and improved cardiac dysfunction after MT (P<0.05). Incubation of cardiomyocytes with TS significantly increased reactive oxygen species ROS and MDA generation (P<0.01). Treatment with GRb1 or ROS scavenger TEMPOL reduced oxidative stress induced by TS and increased cell viability (P<0.05). CONCLUSION GRb1 treatment alleviates oxidative stress induced by MT at an early stage, which reduces secondary cardiac injury and improves cardiac dysfunction after MT.