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抗生素治疗对急性腹膜炎大鼠腹膜组织炎症因子表达及腹膜转运功能的影响 被引量:3

Effects of antibiotic treatment on the inflammatory mediator expression in peritoneum and the peritoneal transport function in the rat with acute bacterial peritonitis
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摘要 目的:观察抗生素治疗对急性腹膜炎大鼠腹膜组织炎症因子的表达及腹膜功能的影响,并初步探讨其影响机制。方法:SD雄性大鼠随机分为3组:对照组(n=28)腹腔注射PBS50mL·kg-1;腹膜炎组(n=28)腹腔注射E.coli3.3×108cfu·kg-1;治疗组(n=28)腹腔注射E.coli3.3×108cfu·kg-1,并于3h、9h腹腔注射庆大霉素10mg·kg-1。在24h、48h、72h、7d分别处死7只大鼠,处死前4h做PET,取腹水、血做细菌培养及白细胞计数,取腹膜组织做病理及NF-κB、CD45、IL-1β、TNF-α的检测。结果:(1)对照组细菌培养阴性,腹膜炎组在24h、48h、72h阳性,治疗组在24h、48h阳性;腹膜炎组血白细胞在24h、48h显著低于对照组,治疗组血白细胞未见显著变化;腹膜炎组腹水白细胞从24h到72h均显著高于对照组,治疗组在24h、48h显著高于对照组,并且在24h显著高于腹膜炎组。(2)活化NF-κB、IL-1β、TNF-α、CD45在对照组为阴性或微弱表达,在腹膜炎组和治疗组从24h至72h均显著高表达,但治疗组在48h、72h显著低于腹膜炎组;IL-1β、TNF-αmRNA水平和蛋白表达相一致。(3)腹膜炎和治疗组的超滤量和D/D0Glu均显著低于对照组,D/PTP均显著高于对照组;治疗组的超滤量及D/D0Glu和腹膜炎组比较无显著差异,但D/PTP显著低于腹膜炎组。结论:有效抗生素治疗可以部分降低腹膜炎大鼠腹膜组织炎症因子的表达,并部分改善腹膜对蛋白的转运功能,但不能有效改善对液体的超滤和葡萄糖的转运功能。 AIM: To observe the effect of antibiotic treatment on the inflammatory mediator expression in peritoneum and the peritoneal transport function in rats with acute peritonitis, and explore its mechanisms. METHODS: Eighty-six SD rats were randomly divided into three groups. Control group (n=28) were treated with PBS (ip), peritonitis group (n=28) and treatment group (n=28) were challenged with the E.coli (ip), but at 3 h and 9 h gentamicin was given (ip) in treatment group. Seven rats of every group were randomly sacrificed at 24 h, 48 h, 72 h and 7 d. Peritoneal equilibration test (PET) was did before they were killed. Leukocyte count, pathological changes and the expression of CD45, NF-κB, IL-1β, TNF-α in peritoneum were examined. RESULTS: (1)The blood leukocytes in peritonitis group decreased strikingly, but did not change obviously in other two groups. The peritoneal fluid leukocytes in peritonitis group increased significantly from 24 h to 72 h, while in treatment group, it enhanced more strikingly than peritonitis group at 24 h, and recovered earlier. (2) Both in peritonitis group and treatment group, the expression of activated NF-κB, IL-1β, TNF-α and CD45 increased significantly, but the treatment group was lower than model group at 48 h and 72 h. The mRNA level of IL-1β and TNF-α had the same trend as their protein expression. (3) Compared with the control group, UF and D/D_0 Glu decreased significantly in model group and treatment group, and D/PTP increased dramatically. The D/P TP in treatment group lowered obviously compared with peritonitis group, while the net UF and D/D_0 Glu had not significant difference between treatment group and model group. CONCLUSION: Antibiotic treatment can partly decrease the expression of inflammatory mediators in peritoneum of rats with acute peritonitis and also can improve the protein transport ability to some extent, but can not improve the peritoneal ultrafiltration and the glucose transport function.
出处 《中国病理生理杂志》 CAS CSCD 北大核心 2005年第7期1298-1304,共7页 Chinese Journal of Pathophysiology
基金 广州市科委重点项目(2004Z2-E0041) 教育部国际合作项目(教外司留[2001]498号)
关键词 腹膜炎 炎症介导素类 庆大霉素类 Peritonitis Proinflammatory mediators Gentamicins
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参考文献14

  • 1Cueto- Manzano AM, Quintana- Pina E, Correa- Rotter R.Long- term CAPD survival and analysis of mortality risk factor: 12 - year experience of a single Mexican center[J]. Perit Dial Int, 2001, 21(2): 148- 153.
  • 2Kazuhiko F, Hideaki S, ILsooH, etal. Concomitant increase in neutrophil adhesion to inflammatory peritoneum and remote organs during peritonitis[J]. J Surg Res, 1999, 81(2): 156- 163.
  • 3Wang T, Qureshi A, Heimburger O, et al. Dioctyl sodium sulphosuccinate increases net ultrafiltration in peritoneal dialysis[J]. Nephrol Dial Transplant, 1997, 12(6): 1218 - 1222.
  • 4Combet S, van Landschoot M, Moulin P, et al. Regulation of aquaporin - 1 and nitric oxide synthase isoformsin a rat model of acute peritonitis[J]. J Am Soc Nephrol, 1999, 10( 10):2185-2196.
  • 5贾占军 余学清 王欣.大鼠急性腹膜炎模型的建立及其对腹膜功能的影响[J].中华肾脏病杂志,2004,20:37-42.
  • 6Gurleyik E, Gurleyik G, Unalmiser S. Blockade of transdiaphragmatic lymphatic absorption reduced systemic inflammatory response syndrome during experimental peritonitis: evaluation with body oxygen kinetics in rats[J]. Eur J Surg, 1996,162(9): 729 - 734.
  • 7Silverman N, Maniatis T. NF- κB signaling pathways in mammalian and insect innate immunity[J]. Genes, 2001, 15(18): 2321-2342.
  • 8Chow JC, Young DW, Golenbock DT, et al. TLR4 mediates LPS- induced signal transduction[J]. J Biol Chem, 1999,274(16): 10689 - 10692.
  • 9Anest V, Hanson JL, Cogswell PC, et al. A nucleosomal function for IκB kinase - a in NF - κB - dependent gene expression[J]. Nature, 2003, 423(6940): 659-663.
  • 10Richmond A. Nf- κB, chemokine gene transcription and tumour growth[J]. Nature Rev Immunol, 2002, 2(9): 664-674.

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