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interleukin-1 receptor antagonist intervenes in signaling between different types of synoviocytes in rats with adjuvant arthritis

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Acta Pharmacologica Sinica 2006年第1期27卷 111-118页

作者： Yong-qiu ZHENG~2 Wei WEI~(2,3,4) Min DAI~2 Lei ZHU~2 Xiao-yi JIA~2 Yuan WANG1 Institute of Clinical Pharmacology,Anhui Medical University.Hefei 230032,China 3 Key Laboratory of Anti-inflammation and Immunopharmacology in Anhui Province,Hefei 230032.China Institute of Clinical Pharmacology Anhui Medical University Hefei China Key Laboratory of Anti-inflammation and Immunopharmacology in Anhui Province Hefei China

Aim:To investigate the mechanisms of interleukin-1 receptor antagonist （IL-1ra）in the treatment of adjuvant arthritis （AA）.Methods:AA was induced in rats bytreatment with Freund's complete adjuvant （FCA）.Rats were given an intracuta-neous injection of IL-1ra （2.5,10,40mg/kg,3 times per day） from d 14 to d 21 *** proliferation and the activity of IL-1 were determinedby using MTT *** necrosis factor alpha （TNF-α） and prostaglandin E2（PGE2） concentrations were measured by *** ultrastructureof synoviocytes was observed by using a transmission electron *** of c-Jun N-terminal kinase （JNK）,extracellular regulating kinase（ERK） and p38 kinase were detected by Western blot ***:IL-1ra （10and 40 mg/kg,ic,d 14-21） modulated the secondary inflammatory reaction（P1）,ultrastructure of synoviocytes and mitogen-activated protein kinase（MAPK） phosphorylation in AA *** administration of IL-1ra （10 and 40mg/kg,ic,d 14-21） in AA rats significantly decreased the production of IL-1,PGE2and TNF-α by macrophage-like synoviocytes （MLS）（P1）.IL-1ra （2.5 mg/kg）also decreased the production of PGE2（P1） and TNF-α（P1ra （10 and 40 mg/kg,ic.d 14-21）.Conclusion:IL-1ra hasanti-inflammatory effects because it modulates the ultrastructure of synoviocytes,decreases the production of pro-inflammatory mediators by MLS,and inhibits thephosphorylation of MAPK in FLS.

关键词： interleukin-1 receptor experimental arthritis mitogen-activated protein kinase synovial membrane

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interleukin-1 receptor is a target for adjunctive control of diazepam-refractory status epilepticus in mice

Interleukin-1 receptor is a target for adjunctive control of...

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中国神经科学学会第十二届全国学术会议

作者： Zheng-Hao Xu Yi Wang An-Feng Tao Jie Yu Xiao-Yu Wang Yun-Yun Zu Shi-Hong Zhang Zhong Chen Laboratory of Brain Function and Disease in Chinese Medicine College of Basic Medical Science Zhejiang Chinese Medical University Department of Pharmacology Key Laboratory of Medical Neurobiology of the Ministry of Health of China College of Pharmaceutical Sciences School of Medicine Zhejiang University

Proinflammatory cytokine interleukin-1 beta（IL-1β） increasingly released and accumulated in the brain during SE, however its role in the progressive refractoriness of status epilepticus（SE） remains controversial. In present study, SE induced by kainic acid（KA） was allowed to continue for 40 min before diazepam administration to induce a prolonged SE. The onset and termination of SE were monitored by electroencephalogram recording of the hippocampus. We found diazepam failed to terminate prolonged SE（both behavioral seizures and ictal EEGs）, although it terminate non-prolonged SE within minutes when given 10 min after the SE onset. The hippocampal expression level of IL-1β during prolonged rather than non-prolonged SE was significantly higher than that of sham control. Administration of recombinant human IL-1β weaken the efficacy of diazepam by prolonging its latency to terminate non-prolonged SE. On the contrary, administration of interleukin-1 receptor antagonist（IL-1 RA） combined with diazepam terminated prolonged SE, although IL-1 RA alone is not capable to terminate prolonged SE. Moreover, prolonged SE was not diazepam-refractory in IL-1 R1 knock-out mice. Thus, the present study provides direct evidence that accumulated IL-1β contributed to the progressive diazepam refractoriness of SE via activating IL-1 R1, and suggest that diazepam combined IL-1 R1 antagonists with may be a novel effective strategy for the control of refractory prolonged SE.

关键词： Status epilepticus Neuroinflammation Epilepsy Diazepam interleukin-1 receptor interleukin-1β

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Conventional, but not remote ischemic preconditioning, reduces iNOS transcription in liver ischemia/reperfusion

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World Journal of Gastroenterology 2014年第28期20卷 9506-9512页

作者： Bergthor Bjornsson Anders Winbladh Linda Bojmar Tommy Sundqvist Per Gullstrand Per Sandstrom Department of Surgery County Council of Ostergotland58185 Linkoping Sweden Department of Clinical and Experimental Medicine Faculty of Health SciencesLinkping University58185 Linkoping Sweden

AIM:To study the effects of preconditioning on inducible nitric oxide synthase(iNOS)and interleukin 1(IL-1)receptor transcription in rat liver ischemia/reperfusion injury(IRI).METHODS:Seventy-two male rats were randomized into 3 groups:the one-hour segmental ischemia(IRI,n=24)group,the ischemic preconditioning(IPC,n=24)group or the remote ischemic preconditioning(RIPC,n=24)*** IPC and R-IPC were performed as 10 min of ischemia and 10 min of *** iNOS and the IL-1 receptor mRNA in the liver tissue was analyzed with real time *** total Nitrite and Nitrate(NOx)in continuously sampled microdialysate(MD)from the liver was *** addition,the NOx levels in the serum were ***:After 4 h of reperfusion,the iNOS mRNA was significantly higher in the R-IPC(ΔCt:3.44±0.57)group than in the IPC(ΔCt:5.86±0.82)group(P=0.025).The IL-1 receptor transcription activity was reduced in the IPC group(ΔCt:1.88±0.53 to 4.81±0.21),but not in the R-IPC group,during reperfusion(P=0.027).In the MD,a significant drop in the NOx levels was noted in the R-IPC group(12.3±2.2 to 4.7±1.2μmol/L)at the end of ischemia compared with the levels in early ischemia(P=0.008).A similar trend was observed in the IPC group(11.8±2.1 to 6.4±1.5μmol/L),although this difference was not statistically *** levels of NOx rose quickly during reperfusion in both ***:IPC,but not R-IPC,reduces iNOS and IL-1 receptor transcription during early reperfusion,indicating a lower inflammatory *** is consumed in the ischemic liver lobe.

关键词： Ischemia-reperfusion injury Preconditioning Remote preconditioning Liver ischemia Liver surgery Microdialysis Nitric oxide Inducible nitric oxide synthase interleukin-1 receptor

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