The protective effects of diallyl trisulfide on liver were examined in rats with sepsis. Sepsis was reproduced in rats by cecum ligation and puncture (CLP). Fifty-six male Wistar rats were randomly divided into sham-o...The protective effects of diallyl trisulfide on liver were examined in rats with sepsis. Sepsis was reproduced in rats by cecum ligation and puncture (CLP). Fifty-six male Wistar rats were randomly divided into sham-operated group (group S, n=8), sepsis model group (group C, n=24), diallyl trisulfide (DATS)-treated group (group D, n=24). Animals in groups C and D were further divided into three subgroups according to different observation time points, with 8 rats in each sub-group.Rats in group D and C were intravenously injected with normal saline or DATS respectively at a dose of 20 mg/kg after the establishment of sepsis model. Eight rats in groups C and D were sacrificed at 3, 6 and 24 h post-CLP and their livers were harvested for detection of interleukin (IL)-1 receptor associated kinase-4 (IRAK-4), nuclear factor-κB (NF-κB), c-fos, c-jun, malondialdehydethhe (MDA) and superoxide dismutase (SOD), tumor necrosis factor alpha (TNF-α) and for pathological examination. The results showed that the levels of serum IRAK-4, NF-κB and TNF-α in hepatic tissues were higher in group C than group S (control group) (P<0.05). After DATS treatment, the levels of IRAK-4 and NF-κB in the hepatic tissues and serum TNF-α in group D were lower than those in group C (P<0.05). The levels of c-fos and c-jun and MDA in the hepatic tissues were higher in group C than in group S (P<0.05). After DATS treatment, the levels of c-fos and c-jun and MDA in the hepatic tissues were significantly lower in group D than in group C (P<0.05). When compared with group S group, concentration of SOD in the hepatic tissues in group C was significantly lower (P<0.05). After DATS treatment, the concentration of SOD in the hepatic tissues was higher in group D than in group C (P<0.05). These findings suggested that treatment with DATS could ameliorate sepsis-induced liver injury in rats. The protective effect might be related to its ability to inhibit the signal pathway of IRAK-4 and NF-κB, thereby decreasing the production of oxygen free radic展开更多
目的:观察脂多糖(LPS)预处理后白细胞介素-1受体相关激酶-4(IRAK-4)表达水平在大鼠肝脏缺血再灌注(I/R)早期的变化,探讨LPS预处理减轻肝脏缺血再灌注损害(I/R I)的相关机制。方法:雄性SD大鼠,随机分为正常对照组,缺血再灌注组(I/R组)和...目的:观察脂多糖(LPS)预处理后白细胞介素-1受体相关激酶-4(IRAK-4)表达水平在大鼠肝脏缺血再灌注(I/R)早期的变化,探讨LPS预处理减轻肝脏缺血再灌注损害(I/R I)的相关机制。方法:雄性SD大鼠,随机分为正常对照组,缺血再灌注组(I/R组)和LPS预处理组(LPS组)。正常对照组未予任何处理;LPS组第1 d经尾静脉给予脂多糖0.1mg.kg-1,第2、3、4、5 d给予0.5 mg.kg-1;I/R组给予等体积0.5 mL无菌PBS液。第8 d,建立肝脏缺血再灌注模型。再灌注后0 m in、60 m in及180 m in,蛋白免疫印记法及逆转录-聚合酶链式反应测定肝组织的IRAK-4蛋白和mRNA表达水平;酶连免疫吸附法检测肝组织NF-κB活性及血清TNF-α含量。结果:再灌注0 m in,IRAK-4蛋白与mRNA表达水平依次为LPS组>I/R组>正常对照组(P<0.01),NF-κB活性以及TNF-α含量LPS组与I/R组差异无显著(P>0.05),但均高于正常对照组(P<0.01);再灌注后60 m in及180m in,LPS组的IRAK-4蛋白与mRNA表达水平,NF-κB活性以及TNF-α含量却明显低于I/R组(P<0.01)。结论:抑制IRAK-4表达是LPS预处理减轻肝脏I/R I的重要机制之一。展开更多
Objective: To investigate the role of interleukin-1 (IL-1) receptor associated kinase-2 (IRAK-2) in IL1 and TNF-stimulated nuclear factor-kappa B (NF-kappa B ) activation. Metbods: The 293 cell was trans fectedwith an...Objective: To investigate the role of interleukin-1 (IL-1) receptor associated kinase-2 (IRAK-2) in IL1 and TNF-stimulated nuclear factor-kappa B (NF-kappa B ) activation. Metbods: The 293 cell was trans fectedwith antisense IRAK-2 oligonucleotide (IRAK-2 ODN) followed by stimulating the cell with IL-1 or tumor necrosis factor (TNF), and then the levels of NF-kappa B activation was analyzed by sandwich enzyme-linked immunosorbent assay (ELISA ). Result: Pre-transfecting with antisense IRAK-2 ODN could remarkably decreasethe levels of NF-kappa B activation stimulated by IL-1 in time- and concentration-dependent manner, it can not attenuate the one stimulated by TNF. Conclusion: The responses of IL-1 and TNF-stimulated NF-kappa B activation to antisense IRAK-2 oligonucleotids were different. IRAK-2 plays a key role in the IL-1 signaling events leading to NF kappa B activation.展开更多
基金supported by grants from the Natural Science Foundation of Hubei Province (No. 2011CDB196)
文摘The protective effects of diallyl trisulfide on liver were examined in rats with sepsis. Sepsis was reproduced in rats by cecum ligation and puncture (CLP). Fifty-six male Wistar rats were randomly divided into sham-operated group (group S, n=8), sepsis model group (group C, n=24), diallyl trisulfide (DATS)-treated group (group D, n=24). Animals in groups C and D were further divided into three subgroups according to different observation time points, with 8 rats in each sub-group.Rats in group D and C were intravenously injected with normal saline or DATS respectively at a dose of 20 mg/kg after the establishment of sepsis model. Eight rats in groups C and D were sacrificed at 3, 6 and 24 h post-CLP and their livers were harvested for detection of interleukin (IL)-1 receptor associated kinase-4 (IRAK-4), nuclear factor-κB (NF-κB), c-fos, c-jun, malondialdehydethhe (MDA) and superoxide dismutase (SOD), tumor necrosis factor alpha (TNF-α) and for pathological examination. The results showed that the levels of serum IRAK-4, NF-κB and TNF-α in hepatic tissues were higher in group C than group S (control group) (P<0.05). After DATS treatment, the levels of IRAK-4 and NF-κB in the hepatic tissues and serum TNF-α in group D were lower than those in group C (P<0.05). The levels of c-fos and c-jun and MDA in the hepatic tissues were higher in group C than in group S (P<0.05). After DATS treatment, the levels of c-fos and c-jun and MDA in the hepatic tissues were significantly lower in group D than in group C (P<0.05). When compared with group S group, concentration of SOD in the hepatic tissues in group C was significantly lower (P<0.05). After DATS treatment, the concentration of SOD in the hepatic tissues was higher in group D than in group C (P<0.05). These findings suggested that treatment with DATS could ameliorate sepsis-induced liver injury in rats. The protective effect might be related to its ability to inhibit the signal pathway of IRAK-4 and NF-κB, thereby decreasing the production of oxygen free radic
文摘目的:观察脂多糖(LPS)预处理后白细胞介素-1受体相关激酶-4(IRAK-4)表达水平在大鼠肝脏缺血再灌注(I/R)早期的变化,探讨LPS预处理减轻肝脏缺血再灌注损害(I/R I)的相关机制。方法:雄性SD大鼠,随机分为正常对照组,缺血再灌注组(I/R组)和LPS预处理组(LPS组)。正常对照组未予任何处理;LPS组第1 d经尾静脉给予脂多糖0.1mg.kg-1,第2、3、4、5 d给予0.5 mg.kg-1;I/R组给予等体积0.5 mL无菌PBS液。第8 d,建立肝脏缺血再灌注模型。再灌注后0 m in、60 m in及180 m in,蛋白免疫印记法及逆转录-聚合酶链式反应测定肝组织的IRAK-4蛋白和mRNA表达水平;酶连免疫吸附法检测肝组织NF-κB活性及血清TNF-α含量。结果:再灌注0 m in,IRAK-4蛋白与mRNA表达水平依次为LPS组>I/R组>正常对照组(P<0.01),NF-κB活性以及TNF-α含量LPS组与I/R组差异无显著(P>0.05),但均高于正常对照组(P<0.01);再灌注后60 m in及180m in,LPS组的IRAK-4蛋白与mRNA表达水平,NF-κB活性以及TNF-α含量却明显低于I/R组(P<0.01)。结论:抑制IRAK-4表达是LPS预处理减轻肝脏I/R I的重要机制之一。
文摘Objective: To investigate the role of interleukin-1 (IL-1) receptor associated kinase-2 (IRAK-2) in IL1 and TNF-stimulated nuclear factor-kappa B (NF-kappa B ) activation. Metbods: The 293 cell was trans fectedwith antisense IRAK-2 oligonucleotide (IRAK-2 ODN) followed by stimulating the cell with IL-1 or tumor necrosis factor (TNF), and then the levels of NF-kappa B activation was analyzed by sandwich enzyme-linked immunosorbent assay (ELISA ). Result: Pre-transfecting with antisense IRAK-2 ODN could remarkably decreasethe levels of NF-kappa B activation stimulated by IL-1 in time- and concentration-dependent manner, it can not attenuate the one stimulated by TNF. Conclusion: The responses of IL-1 and TNF-stimulated NF-kappa B activation to antisense IRAK-2 oligonucleotids were different. IRAK-2 plays a key role in the IL-1 signaling events leading to NF kappa B activation.
