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目的:观察小檗碱(Ber)预防内毒素血症小鼠心功能障碍的作用机制是否与其激活α2肾上腺素能受体有关,并探讨中性粒细胞在其中的作用。方法:将雄性BALB/c小鼠随机分为对照组(control)、脂多糖组(LPS)、小檗碱+LPS组(Ber+LPS)、α2肾上腺素能受体拮抗剂育亨宾+小檗碱+LPS组(Yohimbine+Ber+LPS)、育亨宾+LPS组(Yohimbine+LPS)、小檗碱组、育亨宾+小檗碱(Yohimbine+Ber)组和育亨宾(Yohimbine)组,分别用蒸馏水,小檗碱(50 mg/kg),育亨宾+小檗碱(2 mg/kg+50 mg/kg)或育亨宾(2 mg/kg)灌胃,每天1次,连续3d,第3 d灌胃后1 h,腹腔注射生理盐水或LPS(20 mg/kg)。观察注射LPS后12 h各组小鼠心肌组织结构的改变,用VisualSonies Vevo770TM高分辨小动物超声系统测定小鼠的心功能,并用Western blotting方法测定LPS注射后0.5 h心肌髓过氧化物酶(MPO)的含量。结果:LPS注射后12 h,LPS组小鼠心肌组织出现明显水肿。小檗碱、育亨宾、小檗碱+育亨宾组小鼠心肌的病理改变明显轻于LPS组。超声心动图检测显示,LPS组小鼠心输出量(CO)和每搏量(SV)均显著低于对照组、小檗碱、育亨宾、小檗碱+育亨宾组。腹腔注射LPS后0.5 h,LPS组心肌MPO的含量显著高于对照组,小檗碱、育亨宾+小檗碱组心肌MPO的水平显著低于LPS组,而育亨宾组心肌MPO的含量与LPS组没有显著差别。结论:小檗碱预处理能够减轻内毒素血症小鼠的心功能障碍,其作用机制与其激活α2肾上腺素能受体和抑制LPS引起的心肌中性粒细胞浸润无关,体内α2肾上腺素能受体激活可能在LPS引起的心功能障碍中发挥重要作用。
OBJECTIVE: To investigate whether berberine (Berberine) can prevent cardiac dysfunction in endotoxemia mice and its mechanism of activation of α2 adrenergic receptor and explore the role of neutrophils in it. Methods: Male BALB / c mice were randomly divided into control group, lipopolysaccharide group (LPS), berberine + LPS group (Ber + LPS), α2 adrenergic receptor antagonist yohimbe + Yohimbine + Ber + LPS group, Yohimbine + LPS group, berberine group, Yohimbine + Ber group and Yohimbine group. Groups were given gavage with distilled water, berberine (50 mg / kg), yohimbine + berberine (2 mg / kg + 50 mg / kg) or yohimbine (2 mg / kg) , For 3 consecutive days. The rats were intraperitoneally injected with normal saline or LPS (20 mg / kg) 1 h after the third day. The changes of myocardial tissue structure were observed 12 h after injection of LPS in mice. The heart function of mice was detected by using VisualSonies Vevo770 TM high resolution small animal ultrasound system. The level of myocardial myeloperoxidase (MPO) was measured by Western blotting 0.5 h after LPS injection. ) Content. Results: At 12 h after LPS injection, there was obvious edema in the myocardium in LPS group. The pathological changes of myocardium in berberine, yohimbine and berberine plus yohimbe groups were significantly lighter than those in LPS group. Echocardiography showed that cardiac output (CO) and stroke volume (SV) of mice in LPS group were significantly lower than those in control group, berberine, yohimbine and berberine + yohimbe group. At 0.5 h after intraperitoneal injection of LPS, the content of MPO in LPS group was significantly higher than that in control group. The levels of MPO in berberine and yohimbine + berberine group were significantly lower than those in LPS group, while the MPO content in yohimbin group There was no significant difference with LPS group. Conclusion: Berberine preconditioning can relieve cardiac dysfunction in endotoxemic mice. The mechanism of action is not related to the activation of α2 adrenergic receptor and inhibition of myocardial neutrophil infiltration induced by LPS. The α2 adrenergic receptor Somatic activation may play an important role in cardiac dysfunction caused by LPS.