| SOCSs在慢加急性肝衰竭大鼠肝组织中的表达变化及意义 |
| 投稿时间：2015-01-21 修订日期：2015-02-12 点此下载全文 |
| 引用本文：王柯尹,杨乃彬,倪顺兰,谢新生,余晓,卢明芹.SOCSs在慢加急性肝衰竭大鼠肝组织中的表达变化及意义[J].医学研究杂志,2015,44(10):106-110 |
| DOI：
10.11969/j.issn.1673-548X.2015.10.030 |
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| 中文摘要:目的 探讨细胞因子信号转导抑制因子(suppressors of eytokine signaling,SOCSs)在慢加急性肝衰竭(acute on chronic liver failure,ACLF)大鼠肝组织中的表达及其在ACLF发生中的作用。 方法 健康SD大鼠随机分组,ACLF组大鼠腹腔注射1.5ml/kg的50%四氯化碳花生油溶液,每3天1次,10次后改为2ml/kg,每3天1次,9次后给予250mg/kg D-氨基半乳糖(D-GalN)联合50μg/kg脂多糖(LPS)急性攻击,给药后0、6、12、24h 留取大鼠血及肝组织。血生化检测ALT、AST水平和ELISA法检测TNF-α、IL-6水平。HE染色下观察肝脏病理学变化。RT-PCR检测大鼠肝组织SOCS-1、SOCS-3mRNA表达。 结果 大鼠慢加急性肝衰竭模型复制成功,ACLF组血清ALT和AST水平逐渐上升,在12h升高最明显,血清TNF-α、IL-6水平在造模后0h 即明显高于对照组,至6h达峰值(P<0.05),肝组织SOCS-1、SOCS-3mRNA水平于造模后0h开始升高,12h升高最为显著,之后逐渐下降,与正常对照组相比,各时间点差异有统计学意义(P<0.05)。 结论 SOCSs在慢加急性肝衰竭过程中升高,其变化与TNF-α、IL-6改变相关,提示SOCSs可能参与慢加急性肝衰竭中的炎症及免疫调节过程。 |
| 中文关键词:慢加急性肝衰竭 细胞因子 细胞因子信号转导抑制因子 |
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| Expression of SOCSs in Rats with Acute-on-chronic Liver Failure and Its Significance |
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| Abstract:Objective To investigate the expression of SOCSs in liver tissues of rats with acute on chronic liver failure(ACLF) and the function of SOCSs in ACLF. Methods The SD male rats were randomly divided into two groups. Rats in ACLF group were intraperitoneally injected with: 1.5ml/kg of 50% carbon tetrachloride peanut oil solution, every 3 days for the first month; 2ml/kg of 50% carbon tetrachloride peanut oil solution, every 3 days for another two months; then 250mg/kg D-GalN and 50μg/kg LPS at once. Rats in normal group were intraperitoneally injected with 0.9% NaCl solution. Liver tissue and blood were collected on 0,6,12,24hours after the final injection. The level of ALT、AST were detected by automatic biochemical analyzer and TNF-α,IL-6 were determined by ELISA. The liver pathologic changes were observed with HE staining by microscope. SOCS-1,SOCS-3mRNA of liver tissues were determined by RT-PCR. Results ACLF model of rats were successfully built. The level of ALT and AST in model group peaked at 12 hours. The level of TNF-α,IL-6 were obviously higher than those in control group and peaked at 6h(P<0.05). SOCS-1,SOCS-3mRNA began to rise after modeling,peaked at 12h and decreased gradually. Compared with the normal group, difference in all time point were statistically significant(P<0.05). Conclusion The level of SOCSs in ACLF group were upregulated and the upregulation was associated with IFN-α,IL-6, suggesting that SOCSs may participate in the process of inflammation and immune regulation in ACLF. |
| keywords:Acute-on-chronic liver failure Cytokines Suppressors of cytokine signalings |
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