Ilhan N, Susam S, Gul H F, Bardas R, Ilhan N
Bratisl Lek Listy. 2017;118(5):283-287. doi: 10.4149/BLL_2017_056.
We aimed to investigate the protective effect of selected treatment agents on liver injury in lipopolysaccharide (LPS)-induced rat sepsis model.
The sepsis includes complex inflammatory responses between a microbial pathogen and the host immune system, and leads to organ failure and also death.
This study was performed with 29 male Wistar Albino rats. Rats were divided randomly into five groups: Sham group, LPS-treated sepsis group, LPS+thalidomide treated group, LPS+etanercept treated group and LPS+thalidomide+etanercept treated group, respectively. Liver tissue tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β) and interleukin 6 (IL-6) levels were determined by enzyme-linked immuno-sorbent assay (ELISA) method. The expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) was performed using western blot analysis.
The levels of tissue TNF-α, IL-1β and IL-6 were found statistically significantly higher in sepsis group than in the sham group. TNF-α levels were found statistically significantly decreased in LPS+etanercept and LPS+thalidomide+etanercept treated groups when compared with LPS group (p < 0.05). For IL-1β and IL-6 levels a statistically significant decline was observed in the LPS+thalidomide and LPS+etanercept treated groups compared to the LPS group (p < 0.05). Expression of NF-κB protein in liver tissue was significantly elevated in the LPS group compared to sham group (p < 0.001). In treatment groups, a marked decrease was observed in NF-κB protein expression.
The results of this investigation suggested that etanercept and thalidomide administration may have a beneficial effect on LPS-induced sepsis. So, the present study may have significant clinical relevance, but clinical trials are needed to confirm these results (Tab. 1, Fig. 1, Ref. 36).
我们旨在研究特定治疗药物对脂多糖（LPS）诱导的大鼠脓毒症模型肝损伤的保护作用。
脓毒症包括微生物病原体与宿主免疫系统之间复杂的炎症反应，并导致器官衰竭甚至死亡。
本研究使用29只雄性Wistar白化大鼠。大鼠被随机分为五组：假手术组、LPS诱导的脓毒症组、LPS+沙利度胺治疗组、LPS+依那西普治疗组和LPS+沙利度胺+依那西普治疗组。采用酶联免疫吸附测定（ELISA）法测定肝组织肿瘤坏死因子α（TNF-α）、白细胞介素1β（IL-1β）和白细胞介素6（IL-6）水平。使用蛋白质印迹分析检测活化B细胞核因子κB（NF-κB）的表达。
脓毒症组组织TNF-α、IL-1β和IL-6水平在统计学上显著高于假手术组。与LPS组相比，LPS+依那西普组和LPS+沙利度胺+依那西普治疗组的TNF-α水平在统计学上显著降低（p<0.05）。与LPS组相比，LPS+沙利度胺组和LPS+依那西普治疗组的IL-1β和IL-6水平在统计学上显著下降（p<0.05）。与假手术组相比，LPS组肝组织中NF-κB蛋白表达显著升高（p<0.001）。在治疗组中，观察到NF-κB蛋白表达明显降低。
本研究结果表明，给予依那西普和沙利度胺可能对LPS诱导的脓毒症有有益作用。因此，本研究可能具有重要的临床意义，但需要临床试验来证实这些结果（表1，图1，参考文献36）。
