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低温复苏对失血性休克大鼠肺组织过氧化物酶体增殖物激活受体-γ、诱导性一氧化氮合酶及肿瘤坏死因子-α基因表达的影响 被引量:2

Effects of hypothermia resuscitation on expression of peroxisome proliferator activated receptor gamma, inducible nitric oxide synthase and tumor necrosis factor-α genes in lung tissues of rats with hemorrhagic shock
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摘要 目的观察失血性休克大鼠在不同温度复苏后肺组织内过氧化物酶体增殖物激活受体-γ(PPAR-γ)、诱导性一氧化氮合酶(iNOS)和肿瘤坏死因子-α(TNF-α)基因表达的变化。方法36只成年雄性Wistar大鼠随机平均分为3组:对照组(S)、休克常温复苏组(NR)(37-38℃)和低温复苏组(HR)(33-34℃)。S组只进行外科插管操作,不建立失血性休克模型及复苏,NR组和HR组在建立失血性休克模型后分别在预定温度下进行复苏。实时定量聚合酶链反应(Real—time PCR)检测复苏60min和240min大鼠肺组织PPAR-γ、iNOS和TNF-α mRNA表达变化。结果(1)与对照组比较,复苏60minNR组和HR组PPAR-γ mRNA表达量分别为0.61±0.09和1.71±0.16(P〈0.05)。复苏240minNR组和HR组PPAR-γ mRNA表达量分别为0:54±0.08和2.82±0.19(P〈0.05);(2)与对照组比较,复苏60minNR组和HR组iNOSmRNA表达量分别为3.43±0.27和2.21±0.28(P〈0.05)。复苏240minNR组和HR组iNOSmRNA表达量分别为4.86±0.62和2.93±0.37(P〈0.05);(3)与对照组比较,复苏60minNR组和HR组TNF-α mRNA表达量分别为4.12-±O.30和3.36±0.34(P〈0.05)。复苏240minNR组和HR组TNF-α mRNA表达量分别为5.87±0.34和4.91±0.53(P〈0.05)。结论低温复苏能够上调失血性休克大鼠肺组织PPAR-γ 基因表达。抑制TNF-α和iNOS基因表达,减轻肺组织损伤。 Objective To investigate the effects of different body temperature resuscitation on the expression of peroxisome proliferator activated receptor gamma (PPAR-γ) , inducible nitric oxide synthase (iNOS) and tumor necrosis factor-α(TNF-α) genes in the lung tissue of rats with hemorrhagic shock. Methods Thirty-six adult male Wistar rats were randomly assigned to three groups : control group ( S), normal thermia group (NR) and hypothermia group (HR). Rats in S control group underwent the surgical procedure but were not bled. Rats in NR group and HR group received normal thermia (37-38 ℃ ) resuscitation or hypothermia (33-34 ℃ ) resuscitation respectively during resuscitation and hourly thereafter. Real- time polymerase chain reaction (teal-time PCR) method was used to detect the mRNA expression of PPAR-γ, iNOS and TNF-α in the lung tissutes of rats with hemorrhagic shock after resuscitation for 60 min or 240 min. Results ( 1 ) As compared with S group, PPAR-γ mRNA expression in NR group and HR group was 0. 61 ±0. 09 and 1.71 ±0. 16 respectively (P 〈0.05) after resuscitation for 60 min following hemorrhagic shock and 0. 54 ± 0. 08, and 2. 82 ± 0. 19 ( P 〈 0. 05 ) after resuscitation for 240 min following hemorrhagic shock; (2) As compared with S group, iNOS mRNA expression in NR group and HR group was 3.43 ± 0. 27 and 2. 21 ±0. 28 (P 〈0. 05) after resuscitation for 60 min following hemorrhagic shock, and 4. 86 ± 0. 62 and 2. 93 ± 0. 37 ( P 〈 0. 05 ) after resuscitation for 240 min following hemorrhagic shock ; ( 3 ) As compared with S group, TNF-α mRNA expression in NR group and HR group was 4. 12 ± 0. 30 and 3.36 ± 0. 34 ( P 〈 0. 05 ) after resuscitation for 60 min following hemorrhagic shock, and 5.87 ± 0. 34 and 4. 91 ± 0. 53 (P 〈 0. 05) after resuscitation for 240 min following hemorrhagic shock. Conclusion Hypothermia resuscitation after hemorrhagic shock can raise the PPAR-γ gene expression and inhibit iNOS and TNFα gene expression in the rat lung tissues. Hypothermia resuscitation can reduce the lung tissue damage.
出处 《中华实验外科杂志》 CAS CSCD 北大核心 2013年第1期93-95,F0003,共4页 Chinese Journal of Experimental Surgery
基金 全军“十一五”医药卫生科研基金课题(08G002)
关键词 失血性休克 低温复苏 过氧化物酶体增殖物激活受体-Γ 诱导性一氧化氮合酶 肿瘤坏死因子-Α Hemorrhagic shock Hypothermia resuscitation Peroxisome proliferator activatedreceptor gamma Inducible nitric oxide synthase Tumor necrosis factor-α
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