CRISPLD2蛋白对内毒素-诱导急性呼吸窘迫综合征小鼠炎性因子表达的影响

摘要

目的 探讨CRISPLD2蛋白对内毒素-诱导急性呼吸窘迫综合征(LPS-ARDS)小鼠体内炎性因子表达的影响.方法 采用数字表法将40只雄性昆明小鼠随机分5组:对照组(A组),气道内滴入0.1 mg内毒素(LPS);rCRISPLD2蛋白1组(B组)、rCRISPLD2蛋白2组(C组),小鼠尾静脉分别注射1.0、0.4 mg rCRISPLD2蛋白,6 h后气道内滴入0.1mg LPS;rC-RISPLD2蛋白3组(D组)、rCRISPLD2蛋白4组(E组),予小鼠气道内滴入0.1mg LPS,6 h后予小鼠尾静脉分别注射1.0、0.4 mg rCRISPLD2蛋白.每组小鼠在LPS气道滴入后第12 h收集支气管肺泡灌洗液(BALF),离心后计数沉淀中性粒细胞,测量上清液及血标本中的肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)及IL-6.结果 B、C组BALF中的中性粒细胞计数(0.31±0.07、0.76±0.08)ng/L、TNF-α(8.88±17.37、134.63±24.44)ng/L、IL-1β(48.63±15.61、99.75±12.30)ng/L、IL-6(80.75±21.03、140.12±29.29)ng/L均明显低于A、D、E组(1.64±0.10、1.73±0.13、1.65±0.08),差异有统计学意义(P<0.05);B组以上检测值均明显低于C组,差异有统计学意义(P<0.05).结论 CRISPLD2蛋白可下调LPS所诱导的炎症因子表达水平,并且呈现一定的剂量依赖关系.%Objective To investigate the effect of CRISPLD 2 protein on the expression of inflammatory cytokine in LPS-in-duced acute respiratory distress syndromes ( ARDSs) mice.Methods Forty male Kunming mice were randomly divided into 5 groups;the control group (group A), which was given 0.1mg LPS via the intratracheal instillation;the rCRISPLD2 group 1 (group B) and the rCRISPLD2 group 2 (group C), which were respectively treated with 1mg and 0.4mg rCRISPLD2 by tail vein, and after 6 hours rC-RISPLD2 was injected intratracheally;the rCRISPLD2 group 3 (group D) and the rCRISPLD2 group 4 (group E), which were first given 0.1mg LPS intratracheally and then were injected with 1mg and 0.4mg rCRISPLD2 by tail vein.At hour 12 after intratracheal in-jection of LPS in the mice of all the groups , bronchoalveolar lavage fluid (BALF) was collected.After centrifugation, the number of neutrophils was counted , and the levels of TNF-α, IL-1βand IL-6 were detected in supernatant fluid and blood samples .Results The number of neutrophils(0.31 ±0.07、0.76 ±0.08), TNF-α(8.88 ±17.37、134.63 ±24.44), IL-1β(48.63 ±15.61, 99.75 ±12.30) and IL-6 (80.75 ±21.03,140.12 ±29.29)in serum and BALF in groups B and C were all significantly lower than those of group A , D and E, and statistical significance could be noted , when comparisons were made between these groups (P<0.05).The detected data of group B were obviously lower than those of group C , also with statistical significance (P<0.05).Conclusion rCRISPLD2 could down-regulate the expression levels of LPS-induced inflammatory factors , and dosage dependence could be noted to a certain extent .