舒芬太尼在脂多糖诱导的急性呼吸窘迫综合征大鼠模型中的作用

Effect of sufentanil in lipopolysaccharide-induced acute respiratory distress syndrome rat model

目的观察舒芬太尼在脂多糖诱导的急性呼吸窘迫综合征(ARDS)大鼠模型中的作用及其机制。方法将30只SD大鼠随机分为正常组、模型组和实验组,每组10只。正常组大鼠尾静脉注射生理盐水,模型组大鼠尾静脉注射脂多糖诱导建立大鼠ARDS模型,实验组大鼠建模成功后静脉注射舒芬太尼8μg·kg^(-1)。用酶联免疫吸附(ELISA)法检测大鼠肺泡灌洗液中白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)、白细胞介素-10(IL^(-1)0)炎症因子的水平;原位末端标记(TUNEL)法检测大鼠肺泡上皮细胞凋亡率;以称重法测量大鼠肺组织湿干重比;以蛋白质印迹(Western blot)法检测大鼠肺组织中核因子κB p65(NF-κB p65)蛋白的表达。结果正常组、模型组和实验组大鼠IL-1β水平分别为(37.24±3.81),(164.37±15.87),(67.32±6.83)pg·mL^(-1);IL^(-1)0水平分别为(257.64±26.37),(112.74±13.06),(197.65±20.07)pg·mL^(-1);TNF-α水平分别为(186.35±18.36),(497.62±48.66),(296.39±29.77)pg·mL^(-1);大鼠肺泡上皮细胞凋亡率分别为(2.34±0.03)%,(34.37±3.52)%,(16.87±1.71)%;大鼠肺组织湿/干重比分别为3.67±0.37,8.34±0.91,5.97±0.62;大鼠肺组织中NF-κB p65蛋白的表达分别为1.12±0.13,3.34±0.35,2.63±0.27。以上数据,模型组与正常组比较,实验组与模型组比较,差异均有统计学意义(均P<0.01)。结论舒芬太尼可能通过抑制NF-κB p65蛋白的表达,减轻ARDS大鼠炎症反应、肺组织含水量和细胞凋亡,发挥保护作用。

Objective To investigate the role of sufentanil in of lipopolysaccharide-induced acute respiratory distress syndrome(ARDS) rat model and its mechanism.Methods Thirty SD rats were randomly divided into normal group,model group and experimental group,10 rats in each group.The rats in normal group were injected with normal saline,rats in model group were injected with lipopolysaccharide to induce the establishment of ARDS model.Rats in experimental group were injected with lipopolysaccharide,followed by injected sufentanil 8μg·kg;intravenously.The levels of interleukin-1β(IL-1β),tumor necrosis factor-α(TNF-α) and interleukin-10 (IL-10) in bronchoalveolar lavage fluid were measured by enzyme-linked immunosorbent assay (ELISA).The apoptosis rate of alveolar epithelial cells was detected by TdT mediated dUTP nick end labeling(TUNEL) method;the wet-dry weight ratio of lung tissues was measured by weighing method;the expression of nuclear factorκB p65 (NF-κB p65) protein in rat lung tissues was detected by Western blot assay.Results The levels of IL-1βin normal,model and experimental groups of rats were (37.24±3.81),(164.37±15.87),(67.32±6.83) pg·m L;,respectively;the levels of IL-10 were(257.64±26.37),(112.74±13.06),(197.65±20.07) pg·m L;,respectively;the levels of TNF-αwere(186.35±18.36),(497.62±48.66),(296.39±29.77) pg·m L;,respectively;the apoptosis rates of alveolar epithelial cells were (2.34±0.03)%,(34.37±3.52)%,(16.87±1.71)%,respectively;the wet/dry weight ratio of rat lung tissue were 3.67±0.37,8.34±0.91,5.97±0.62;the expression of NF-κB p65 protein in rat lung tissue were 1.12±0.13,3.34±0.35,2.63±0.27,respectively.For the above data,the differences were statistically significant between model group and normal group,as well as between experimental group and model group(all P<0.01).Conclusion Sufentanil inhibits the inflammatory response,lung tissue water content and cell apoptosis of ARDS rats by inhibiting NF-κB p65protein expression.