出 处:《中华急诊医学杂志》2016年第6期746-750,共5页Chinese Journal of Emergency Medicine
摘 要:目的探索内源性二氧化硫(sulfurdioxide,SO2)对脓毒症大鼠所致急性肺损伤过程炎性介质的调节作用。方法雄性SpragueDawley大鼠24只随机(随机数字法)被分人假手术对照组(control组),假手术+s0:组(s0:组),脓毒症组(sepsis组),脓毒症+SO2组(sepsis+s0:组),每组6只。通过肺组织损伤半定量评分(Indexofquantitativeassessment,IQA)及肺组织湿干质量比(wet/dryweightratio,W/D)对肺损伤进行评价。检测血浆s0:、白细胞介素6、8及10(interleukins-6,IL6、interleukins-8,IL8、interleukins-10,IL10)及单核细胞趋化蛋白-1(Monocytechemotaeticprotein-1,MCP-1)、肿瘤坏死因子d(tumornecrosisfactor—α,TNF-α)含量。结果脓毒症大鼠IQA及W/D与对照组相比显著升高(P均〈0.01),给予SO2干预后显著降低(P均〈0.01)。血浆s02含量在脓毒症组(3.17±3.44)μmol/L与对照组(5.87±1.96)μmol/L下降,给予SO2干预后显著升高(9.78±3.26)μmol/L,P〈0.01;血浆IL6、IL8、IL10及MCP-1、TNF-α含量在脓毒症组分别为(87.08±22.03)、(79.82±19.69)、(66.38±21.77)、(157.58±42.36)及(65.04±19.42)pg/mg,对照组分别为(47.41±9.64)、(42.25±8.16)、(31.96±4.63)、(67.65±10.18)及(33.83±5.75)相比显著升高(P均〈0.01);给予SO2干预后分别为(66.01±16.52)、(61.52±18.32)、(45.61±16.47)、(117.86±34.20)及(61.49±15.33)pg/mg降低(IL6及IL8,P均〈0.05,IL10及MCP-1,P均〈0.01)。结论在脓毒症所致肺损伤的发病过程中,内源性SO2可以通过抑制MCP-1、TNF—α进而减轻炎症因子的表达起到保护作用。Objective The present study was undertaken to examine the regulatory effect of endogeous sulfur dioxide ( SO2 ) on intefleukins in rats with acute lung injury (ALI ) induced by sepsis. Methods Twenty Two male Sprague Dawley (SD) rats were randomly (random number) divided into sham group (Control group), sham + SO2 donor (Na2SO3/NaHSO3, 0. 54 mmol/kg: 0. 18 mmoL/kg) group (SO2 group), sepsis induced ALI group (sepsis group) and sepsis induced ALI with sulfur dioxide pretreatment group ( sepsis + SO2 group ) . Index of quantitative assessment of histological lung injury (IQA) , wet/dry weight ratio (W/D) and the level of SO2 in plasma were measured. IL-6, IL-8, IL 10, MCP-I and TNF-α were measured by ELISA. Results The IQA score and W/D ratio of lung tissues significantly increased in sepsis rats compared with control group ( all P 〈 0. 01 ), but significantly decreased in sulfur dioxide pretreatment rats compared with in sepsis rats ( all P 〈 0. 01 ) . The level of SO2 in plasma decreased in sepsis rats ( 3.17 ± 3.44 ) μmol/L compared with control group (5.87± 1.96)μmol/L, but significantly increased in sulfur dioxide pretreatment rats ( 9.78 ± 3.26 ) μ mol/L compared with in sepsis rats (P 〈0. 01 ) . The level of IL-6, IL-8, IL-10, MCP-1 and TNF-α significantly increased in sepsis rats [ (87.08 ±22.03) pg/mg, (79.82 ± 19. 69) pg/mg, (66.38 ±21.77) pg/mg, ( 157.58 ±42.36 ) pg/mg and ( 65.04 ± 19.42 ) pg/mg, respectively compared with control group [ (47.41±9.64) pg/mg, (42.25±8.16) pg/mg, (31.96±4.63) pg/mg, (67.65±10.18) pg/mg and ( 33.83±5.75 ) pg/mg] ( all P 〈 0. 01 ) . but the level of IL-6, IL-8, IL-10 significantly decreased in sulfur dioxide pretreatment rats [ ( 66.01 ±16. 52 ) pg/mg, ( 61.52 ± 18.32 ) pg/mg and ( 45.61 ± 16.47) pg/mg, respeefively compared with sepsis group ( all P 〈 0.05) . The level of MCP-1 significantly decreased in sulf
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