人参皂苷素Rb1通过减轻氧化应激改善大鼠机械创伤诱发的迟发性心脏功能下降

目的 探讨人参皂苷素Rb1（GRb1）对大鼠机械创伤（MT）所致的迟发性心脏功能下降的保护作用。 方法 利用Nobel-Collip创伤仪制备大鼠MT模型，将大鼠随机分为假手术组（Sham）、创伤模型（MT+Vehicle，MT+V）组、创伤GRb1治疗（MT+GRb1）组，检测各组心脏功能、超氧化物歧化酶（SOD）以及丙二醛（MDA）含量的变化；分离培养大鼠乳鼠心肌细胞，将心肌细胞与各组大鼠血清孵育24 h并给予GRb1或超氧阴离子清除剂（TEMPOL）处理，分为对照（SS）组、创伤血清（TS）组、创伤血清+GRb1处理（TS+GRb1）组、创伤血清+TEMPOL处理（TS+TEMPOL）组，检测细胞存活率以及活性氧（ROS）、乳酸脱氢酶（LDH）和MDA含量的变化。 结果 与Sham组相比，MT后2 h大鼠心肌组织中SOD活性显著下降（P<0.01）、MDA水平升高（P<0.01）；MT后24 h心脏功能明显受损，表现为LVDP、±dP/dt_max均显著下降（P<0.01）。给予GRb1治疗可增强心肌组织中SOD活性（P<0.01）、降低MDA水平（P<0.01），进而改善心脏功能（P<0.05）。对于离体分离培养的大鼠心肌细胞，创伤大鼠血清处理24 h显著增加细胞内ROS和MDA的含量（P<0.01）；利用TEMPOL或者GRb1处理均可减轻（P<0.05）创伤大鼠血清诱导的氧化应激并促进心肌细胞存活。 结论 GRb1通过减轻MT早期诱发的心肌细胞氧化应激保护心肌细胞，进而改善MT导致的迟发性心脏功能下降。

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.