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®世界华人消化杂志2006年7月8日;14(19):1916-1920 wcjd@wjgnet.comISSN1009-3079CN14-1260/R 研究快报RAPIDCOMMUNICATION 雷帕霉素抑制JAK/STAT通路对急性肝损伤大鼠肝组织 HMGB1表达的影响 张芸,赵中夫,韩德五,王锋,许瑞龄,刘明社 ■背景资料张芸,赵中夫,刘明社,山西长治医学院肝病研究所山西省tionofalanineaminotransferase(ALT)leveland 长治市046000 近年的研究发现,HMGB1expression,respectively. 内毒素和细胞因韩德五,王锋,许瑞龄,山西医科大学肝病研究所山西省太 子等刺激巨噬细原市030001 通讯作者:赵中夫,046000,山西省长治市解放东街161号,长治 胞时,HMGB1这RESULTS:Incomparisonwiththatinthenor- 医学院肝病研究所.zhaozf_1226@163.com 种能对DNA重电话:0355-3012335传真:0355-3034065malcontrols(1.00±0.02),HMGB1expression 组、修复、复制收稿日期:2006-03-20接受日期:2006-05-08wassignificantlyincreasedinlivertissues24, 和基因转录起重 要作用的核内结48and72hafterALI(3.12±0.06,3.9±0.08,2.83 构蛋白会被释放±0.04,respectively,t=16.01,3.86,10.46,allP 到胞外,介导炎症Rapamycin-inducedinhibition<0.01),andserumALTlevelsweremarkedly 反应.JAK/STATofJanuskinase/signalelevated.TheexpressionofHMGB1inlivertis- 通路是多种细胞 因子发挥作用的transducerandactivatorofsueswasdramaticallyinhibited24,48and72h 重要信号通路.transcriptionpathwayaffectsafterRPMtreatmentascomparedwiththatin HMGB1是否通过expressionofhigh-mobilityALIgroup(1.67±0.05vs3.12±0.06;1.93±0.06 JAK/STAT通路参 与急性肝损伤病groupbox1inratswithacutevs3.9±0.08;1.47±0.04vs2.83±0.04;t=20.11, 理过程目前尚不liverinjury41.90,26.02,allP<0.01).Inaddition,serum 完全清楚.ALTlevelswerealsomarkedlyreducedduring YunZhang,Zhong-FuZhao,De-WuHan,FengWang,24-72hafterRPMtreatment(P<0.01).HMGB1 Rei-LingXu,Ming-SheLiuexpressionwaspositivelycorrelatedwithALT level(r=0.741,P<0.01). YunZhang,Zhong-FuZhao,Ming-SheLiu,Instituteof Hepatology,ChangzhiMedicalCollege,Changzhi046000,CONCLUSION:TheactivationofJAK/STAT ShanxiProvince,Chinapathwaymaybeinvolvedintheup-regulation De-WuHan,FengWang,Rei-LingXu,InstituteofHepa- tology,ShanxiMedicalUniversity,Taiyuan030001,ShanxiofHMGB1expressioninALI.RPMtreatment Province,Chinacanmarkedlydown-regulatesHMGB1expres- Correspondenceto:ProfessorZhong-FuZhao,InstitutesionandattenuatesALI. ofHepatology,ChangzhiMedicalCollege,161JiefangEast Road,Changzhi046000,ShanxiProvince, China.zhaozf_1226@163.comKeyWords:High-mob