红景天苷对LPS诱导大鼠心肌损伤的保护作用及机制研究

The Protective Effect and Mechanism of Salidroside on LPS Induced Rat Myocardial Injury

研究红景天苷(Salidroside)对脂多糖(LPS)致大鼠心肌损伤的保护作用及机制。雄性清洁级SD大鼠50只,随机分组,分为对照组(NS)10只、LPS模型组(10 mg/kg)10只、红景天苷小剂量(Sal 5 mg/kg)组10只,红景天苷中剂量(Sal 20 mg/kg)组10只,红景天苷大剂量(Sal 50 mg/kg)组10只。腹腔注药后6 h测定左心室收缩压(LVSP)、左心室内压上升及下降最大变化速率(±dp/dtmax)等心功能指标。采用ELISA法和Western blot法测定TNF-α、Toll样受体4和核因子κB蛋白表达。结果显示:与对照组比较,LPS可明显抑制大鼠左室功能,显著增加大鼠心肌TNF-α、TLR4和NF-κB的表达。而与模型组比较,红景天苷可剂量依赖性地下调心肌TLR4、NF-κB及TNF-α表达,改善大鼠左室功能。可见,红景天苷对LPS诱导的大鼠心肌损伤具有一定的保护作用,其机制与抑制TLR4-NFκB-TNFα炎症信号转导通路密切相关。

To investigate the protective effect and mechanism of salidroside on lipopolysaccharides （LPS）-in- duced myocardial injury in rat, 50 male rats were randomly divided into five groups, including 10 in control group （ NS）, 10 in LPS group（ I0 mg/kg）, 10 in salidroside low-dose group（ Sal 5 mg/kg）, 10 in salidroside moderate- dose group（Sal 20 mg/kg） and l0 in salidroside high-dose group （Sal 50 mg/kg）. The functional indexes of heart, such as left ventricular systolic pressure （LVSP） and rise and decline of the maximum velocity of intravent- ricular pressure （ ± dp/dtmax） were examined 6 h after administration of vehicle and salidroside. TNF-α, toll-like receptor 4（TLR4） and nuclear factor kB（NF-KB） protein expression were determined by Western blot and ELISA assay. From results, LPS could increase the expressions of TNF-α, TLR4 and NF-KB, and inhibited the function of rat left ventricle compared with the control group. Also, salidroside upregulated the expression of TNF-α, TLR4 and NF-KB, and improve the function of rat left ventricle compared with the LPS model group. Thus, salidroside plays a pivotal role in protecting myocardial against the LPS-induced injury, and the mechanism may be associated with the inhibition of TLR4-NF-KB signal transduction pathway.