中文摘要：

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3 d,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（R） 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.

英文摘要：

AIM： Berberine （Ber） has been reported to prevent lipopolysaccharide （LPS） -induced cardiac dysfunction, reduce neutrophil infiltration and activate α22 adrenoceptor. The present study was designed to determine whether α22 adrenoceptor activation and inhibition of neutrophil infiltration by Ber are involved in the improvement of LPS - induced cardiac dysfunction. METHODS ： The mice were randomly divided into control, LPS, Ber ＋ LPS, Ber ＋ yohimbine （α22 adrenoceptor antagonist） ＋ LPS, yohimbine ＋ LPS, Ber, Bet ＋ yohimbine and yohimbine groups. Water, Ber （50 mg/kg）, Ber ＋ yohimbine （50 mg/kg ＋ 2 mg,/kg） or yohimbine （2 mg/kg） was given intragastrically once a day for 3 days. Normal saline or LPS （20 rng/kg） was injected intraperitoneally 1 h after intragastrical treatment on day 3. 12 h after LPS injection, the cardiac functions were determined by the technique of high - resolution ultrasonography. The histopathological changes of the myocardium were observed under microscope. Furthermore, the myocardial myeloperoxidase （MPO） was determined by Western blotting. RESULTS ： Pretreatment with Ber, Ber combined with yohimbine or yohimbine atten- uated histopathological changes in the heart of LPS - challenged mice. Echocardiography evaluation demonstrated that LPS decreased the cardiac output and stroke volume at 12 h after LPS challenge, which were reversed by pretreatment with Ber, Ber combined with yohimbine or yohimbine significantly. Compared to control group, LPS increased the level of myocardial MPO. Pretreatment with Ber and Ber combined with yohimbine, but not yohimbine alone significantly reduced the amount of myocardial MPO. CONCLUSION： The improvement of cardiac dysfunction by Ber is independent of ct2 adrenoceptor activation and neutrophil infiltration inhibition in endotoxemic mice. The activation of α2 adrenoceptor by Ber may contribute to the pathogenesis of LPS - induced cardiac dysfunction in mice.