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目的 观察急性胰腺炎(AP)小鼠对脂多糖(LPS)的耐受性并探讨其可能机制。方法 210只C57BL/6J小鼠分为生理盐水(NS)+LPS组(n=105)和AP+LPS组(n=105),两组均以不同LPS剂量分为7个亚组。AP模型制备采用间隔1 h腹腔内注射雨蛙肽(50μg/kg),共7次,于第1次雨蛙肽注射后6 h腹腔内注射LPS;NS+LPS组以NS代替雨蛙肽。每个亚组随机分出10 只观察7 d死亡率,其余5只于第1 次雨蛙肽注射后12 h处死,留取血清及肝、肺、肾、胰腺等组织,检测血清淀粉酶(AMS)、乳酸脱氢酶(LDH)水平及各脏器病理学改变。应用含12 489条小鼠全长基因的寡核苷酸芯片分别检测NS+LPS(15 mg/kg)亚组和AP+ LPS(15 mg/kg)亚组小鼠血白细胞基因表达谱并重复3次,筛选两组间的表达差异基因。结果 NS+LPS组和AP+LPS组死亡率均随LPS剂量增加逐步升高,AP+LPS组死亡率均显著低于同等LPS剂量的NS+LPS组(P<0.05)。AP+LPS组LDH水平明显低于相同LPS剂量的NS+LPS组(P<0.05),而AMS水平显著高于相同LPS剂量的NS+LPS组(P<0.05)。AP+LPS组肝、肺、肾组织损伤较相同LPS剂量的NS+LPS组明显减轻。基因芯片筛选结果显示,AP+LPS(15 mg/kg)亚组与NS +LPS(15 mg/kg)亚组相比炎症反应基因、细胞内信号传导基因、转录调节基因表达下调。结论 AP可增强小鼠对LPS耐受性,其可
Objective To observe the tolerance of lipopolysaccharide (LPS) in acute pancreatitis (AP) mice and explore its possible mechanism. Methods 210 C57BL / 6J mice were divided into seven groups: NS + LPS group (n = 105) and AP + LPS group (n = 105). AP model was prepared by intraperitoneal injection of melatonin (50μg / kg) at an interval of 1 h for 7 times. LPS was injected intraperitoneally 6 h after injection of the first melatonin. NS + LPS group was replaced by NS. In each subgroup, 10 rabbits were randomly assigned to death for 7 days. The remaining 5 rabbits were sacrificed 12 hours after the injection of the first frog peptide. Serum and liver, lung, kidney and pancreas tissues were collected and serum amylase (AMS ), Lactate dehydrogenase (LDH) levels and pathological changes of various organs. The gene expression profiles of white blood cells in NS + LPS (15 mg / kg) subgroup and AP + LPS (15 mg / kg) subgroup were detected by oligonucleotide microarrays with 12 489 full-length genes and repeated 3 Second, screening the difference between the two groups of genes. Results The mortality of NS + LPS group and AP + LPS group increased gradually with the increase of LPS dose. The mortality of AP + LPS group was significantly lower than that of NS + LPS group (P <0.05). The level of LDH in AP + LPS group was significantly lower than that in NS + LPS group (P <0.05), while the level of AMS in AP + LPS group was significantly higher than that in NS + LPS group (P <0.05). The damage of liver, lung and kidney in AP + LPS group was significantly reduced compared with NS + LPS group with the same dosage of LPS. Gene chip screening showed that the expression of inflammatory genes, intracellular signal transduction genes and transcriptional regulation genes were down-regulated in AP + LPS (15 mg / kg) subgroup compared with NS + LPS (15 mg / kg) subgroup. Conclusion AP can enhance mice tolerance to LPS, which can be