TLR2 mRNA upregulation in ischemic lobes in mouse partial hepatic ischemia/reperfusion injury model

J Huazhong Univ Sci Technolog Med Sci. 2004;24(2):144-6. doi: 10.1007/BF02885414.

Abstract

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 (deltaCt: 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 microm/L vs 30 +/- 5 microm/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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Liver / blood supply*
  • Liver / metabolism
  • Male
  • Mice
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • RNA, Messenger / physiology
  • Reperfusion Injury / etiology
  • Reperfusion Injury / metabolism*
  • Toll-Like Receptor 2 / biosynthesis*
  • Toll-Like Receptor 2 / genetics
  • Toll-Like Receptor 2 / physiology
  • Up-Regulation

Substances

  • RNA, Messenger
  • Toll-Like Receptor 2