TLR2 mRNA Upregulation in Ischemic Lobes in Mouse Partial Hepatic Ischemia/Reperfusion Injury Model  

作　　者：张进祥 吴河水 王琳 张锦辉 王慧 郑启昌 

机构地区：[1]Department of Emergency Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology [2]Department of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology [3]Department of General Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology [4]Hereditary Department, Tongji Medical College, Huazhong University of Science and Technology

出　　处：《Journal of Huazhong University of Science and Technology(Medical Sciences)》2004年第2期144-146,共3页华中科技大学学报（医学英德文版）

基　　金：ThisprojectwassupportedbyagrantfromNationalNaturalSciencesFoundationofChina (No .30 2 0 0 2 72 )

摘　　要：To investigate TLR2 (Toll-like receptor 2) mRNA expression in ischemic hepatic lobes under the condition of partial hepatic ischemia/reperfusion injury in BALB/c mice and its relationship with liver function impairment. A partial ischemia/reperfusion injury model was established. The portal vein and hepatic artery supply to the median and left lobes of the liver were obstructed by an atraumatic artery micro-clip, with the obstruction lasting for about 60 min. Then reperfusion was fulfilled by removal of the clip. The liver samples were collected at the 4th h after the restoration of blood inflow. Total RNA was extracted from the liver samples and analyzed quantitatively by method of real-time PCR. At the same time, portal vein serum and plasma were taken respectively for further detection of the level of endotoxin, tumor necrosis factor alpha (TNF-alpha) and plasmic alanine aminotransferase (pALT). The results indicated that TLR2 mRNA in ischemic lobe was up-regulated markedly in mice partial liver ischemia/reperfusion injury model compared to that in sham operation group (ΔCt: 1.05±1.02 vs 5.08±1.36, P<0.001). The level of portal vein pALT and TNF-alpha increased significantly (112.32±17.56 pg/ml vs 6.07±5.33 pg/ml,P<0.01;890±127 μ/L vs 30±5 μ/L, P<0.001) . However, the level of portal vein endotoxin remained below the normal line, suggesting a state of non-endotoxemia. TLR2 mRNA expression in ischemic lobe, as well as portal vein pALT and TNF-alpha, was up-regulated in the model of mice partial ischemia/reperfusion injury, suggesting the involvement of TLR2 in ischemia/reperfusion pathological process.To investigate TLR2 (Toll-like receptor 2) mRNA expression in ischemic hepatic lobes under the condition of partial hepatic ischemia/reperfusion injury in BALB/c mice and its relationship with liver function impairment. A partial ischemia/reperfusion injury model was established. The portal vein and hepatic artery supply to the median and left lobes of the liver were obstructed by an atraumatic artery micro-clip, with the obstruction lasting for about 60 min. Then reperfusion was fulfilled by removal of the clip. The liver samples were collected at the 4th h after the restoration of blood inflow. Total RNA was extracted from the liver samples and analyzed quantitatively by method of real-time PCR. At the same time, portal vein serum and plasma were taken respectively for further detection of the level of endotoxin, tumor necrosis factor alpha (TNF-alpha) and plasmic alanine aminotransferase (pALT). The results indicated that TLR2 mRNA in ischemic lobe was up-regulated markedly in mice partial liver ischemia/reperfusion injury model compared to that in sham operation group (ΔCt: 1.05±1.02 vs 5.08±1.36, P<0.001). The level of portal vein pALT and TNF-alpha increased significantly (112.32±17.56 pg/ml vs 6.07±5.33 pg/ml,P<0.01;890±127 μ/L vs 30±5 μ/L, P<0.001) . However, the level of portal vein endotoxin remained below the normal line, suggesting a state of non-endotoxemia. TLR2 mRNA expression in ischemic lobe, as well as portal vein pALT and TNF-alpha, was up-regulated in the model of mice partial ischemia/reperfusion injury, suggesting the involvement of TLR2 in ischemia/reperfusion pathological process.

关 键 词：toll-like receptor 2 reperfusion injury ENDOTOXIN liver 

分 类 号：R363[医药卫生—病理学]