医学研究杂志
醫學研究雜誌
의학연구잡지
Journal of Medical Research
2015年
10期
106-110
,共5页
王柯尹%杨乃彬%倪顺兰%谢新生%余晓%卢明芹
王柯尹%楊迺彬%倪順蘭%謝新生%餘曉%盧明芹
왕가윤%양내빈%예순란%사신생%여효%로명근
慢加急性肝衰竭%细胞因子%细胞因子信号转导抑制因子
慢加急性肝衰竭%細胞因子%細胞因子信號轉導抑製因子
만가급성간쇠갈%세포인자%세포인자신호전도억제인자
Acute-on-chronic liver failure%Cytokines%Suppressors of cytokine signalings
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 chro-nic 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.
目的 探討細胞因子信號轉導抑製因子(suppressors of eytokine signaling,SOCSs)在慢加急性肝衰竭(acute on chro-nic liver failure,ACLF)大鼠肝組織中的錶達及其在ACLF髮生中的作用. 方法 健康SD大鼠隨機分組,ACLF組大鼠腹腔註射1.5ml/kg的50%四氯化碳花生油溶液,每3天1次,10次後改為2ml/kg,每3天1次,9次後給予250mg/kg D-氨基半乳糖(D-GalN)聯閤50μg/kg脂多糖( LPS)急性攻擊,給藥後0、6、12、24h留取大鼠血及肝組織. 血生化檢測ALT、AST水平和ELISA法檢測TNF-α、IL-6水平. HE染色下觀察肝髒病理學變化. RT-PCR檢測大鼠肝組織SOCS-1、SOCS-3mRNA錶達. 結果 大鼠慢加急性肝衰竭模型複製成功,ACLF組血清ALT和AST水平逐漸上升,在12h升高最明顯,血清TNF-α、IL-6水平在造模後0h即明顯高于對照組,至6h達峰值(P<0.05),肝組織SOCS-1、SOCS-3mRNA水平于造模後0h開始升高,12h升高最為顯著,之後逐漸下降,與正常對照組相比,各時間點差異有統計學意義(P<0.05). 結論 SOCSs在慢加急性肝衰竭過程中升高,其變化與TNF-α、IL-6改變相關,提示SOCSs可能參與慢加急性肝衰竭中的炎癥及免疫調節過程.
목적 탐토세포인자신호전도억제인자(suppressors of eytokine signaling,SOCSs)재만가급성간쇠갈(acute on chro-nic liver failure,ACLF)대서간조직중적표체급기재ACLF발생중적작용. 방법 건강SD대서수궤분조,ACLF조대서복강주사1.5ml/kg적50%사록화탄화생유용액,매3천1차,10차후개위2ml/kg,매3천1차,9차후급여250mg/kg D-안기반유당(D-GalN)연합50μg/kg지다당( LPS)급성공격,급약후0、6、12、24h류취대서혈급간조직. 혈생화검측ALT、AST수평화ELISA법검측TNF-α、IL-6수평. HE염색하관찰간장병이학변화. RT-PCR검측대서간조직SOCS-1、SOCS-3mRNA표체. 결과 대서만가급성간쇠갈모형복제성공,ACLF조혈청ALT화AST수평축점상승,재12h승고최명현,혈청TNF-α、IL-6수평재조모후0h즉명현고우대조조,지6h체봉치(P<0.05),간조직SOCS-1、SOCS-3mRNA수평우조모후0h개시승고,12h승고최위현저,지후축점하강,여정상대조조상비,각시간점차이유통계학의의(P<0.05). 결론 SOCSs재만가급성간쇠갈과정중승고,기변화여TNF-α、IL-6개변상관,제시SOCSs가능삼여만가급성간쇠갈중적염증급면역조절과정.
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 intraper-itoneally injected with:1.5ml/kg of 50%carbon tetrachloride peanut oil solution , every 3 days for the first month;2ml/kg of 50%car-bon 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 lev-el 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 .