和厚朴酚对小鼠脓毒症心肌损伤的保护作用

Protective effects of honokiol treatment on sepsis-induced cardiac injury of mice

探究和厚朴酚(HKL)处理能否减轻小鼠脓毒症心肌损伤及其具体机制。通过小鼠盲肠结扎穿孔24 h建立脓毒症心肌损伤模型。实验小鼠随机分为以下4组:假手术组(Sham组);单纯HKL处理组(HKL组);盲肠结扎穿孔组(CLP组);盲肠结扎穿孔+HKL处理组(CLP+HKL组)。盲肠结扎穿孔24h后检测心脏收缩功能,血清LDH水平,心肌组织活性氧(ROS)产量,丙二醛(MDA)水平,超氧化物歧化酶(SOD)活性,谷胱甘肽过氧化物酶(GSH-Px)活性,心肌凋亡率,Bax,Bcl-2和Caspase-3蛋白表达情况。与CLP组相比,HKL处理组心脏收缩功能显著改善,血清LDH水平、心肌ROS产量、MDA含量、凋亡率、Bax与Caspase-3表达水平显著降低,而Bcl-2表达水平、SOD与GSH-Px活性显著增高(均P <0. 05)。该实验证实HKL处理可通过抑制脓毒症诱发的心肌氧化应激和凋亡,最终减轻脓毒症心肌损伤。

To investigate the protective effects and underlying mechanisms of honokiol(HKL)treatment on cardiac injury induced by sepsis in adult C57BL/6mice.The mice were subjected to cecal ligation and puncture for24h to establish the acute cardiac injury model.The mice were randomly divided into four groups:the Sham,HKL,CLP,and CLP+HKL groups.Twenty-four hours after the surgery,cardiac contractile function,serum lactic dehydrogenase(LDH)level,myocardial reactive oxygen species(ROS)production,malonaldehyde(MDA)content,the activities of superoxide dismutase(SOD)and glutathione peroxidase(GSH-Px),apoptotic ratio and the expression levels of Bax,Bcl-2and Caspase-3were measured in each group.Compared with the CLP group,HKL treatment improved cardiac contractile function,decreased serum LDH level,ROS production,MDA content,the apoptotic ratio and the expression levels of Bax and Caspase-3,and increased the activities of SOD and GSH-Px and the expression level of Bcl-2in heart tissues.This study confirms that HKL treatment could effectively attenuate acute cardiac injury induced by sepsis through reducing oxidative stress and apoptosis.