Abstract: 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.