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[TLR4 is involved in hepatic ischemia/reperfusion injury in mice].
Zhonghua Gan Zang Bing Za Zhi. 2003 Jul; 11(7):424-6.ZG

Abstract

OBJECTIVES

To explore the role of TLR4 in the mechanism of hepatic ischemia/reperfusion (I/R) injury in mice.

METHODS

Wild-type (C3H/Heouj) mice and TLR4 deficient mice (C3H/Hej) were used to prepare the models of liver I/R injury. Partial hepatic ischemia was produced by inflow causing occlusion in the median and left lobes for 45 minutes. Blood was drawn to kill the mice at 1 hours and 3 hours after reperfusion. The blood was used to analyze aspartate aminotransferase (AST) and tumor necrosis factor-alpha (TNFalpha). TNF-alpha mRNA expression and myeloperoxidase (MPO) level in ischemic lobes was examined by northern blot and myeloperoxidase assay, respectively.

RESULTS

AST levels were significantly lower in TLR4 deficient mice, compared with those in wild-type mice at both time points (661.83U/L+/-106.09U/L vs. 1215.5U/L+/- 174.03U/L, t=-6.65, P<0.01; 1145.17U/L+/-132.42U/L vs. 2958.17U/L+/-186.81U/L, t=-5.57, P<0.01). Serum TNF-alpha level was lower in TLR4 deficient mice at 3 hours after reperfusion compared with that in wild-type mice (152.39pg/ml+/-43.3 pg/ml vs. 249.12pg/ml+/-51.89pg/ml, t=-3.13, P<0.05). This difference appeared to be mediated at the gene level, since TNF-alpha mRNA expression had decreased in TLR4 deficient mice at 1 hours after reperfusion, compared with that in wild type mice (80.3+/-28.8 vs. 189.4+/-24.6, t=-3.25, P<0.05). MPO level in ischemic lobes in TLR4 deficient mice at 3 hours after reperfusion was significantly lower than that in wild type mice (F=33.49, P<0.01).

CONCLUSIONS

I/R hepatic injury in TLR4 deficient mice is less than that in wild-type mice. TNF-alpha expression down-regulated at the mRNA level appears critical. These suggest that TLR4 be involved in the mechanism of hepatic ischemia/reperfusion injury in mice.

Authors+Show Affiliations

Department of General Surgery, Union Hospital, Tongji Medical College, Huazhong Science and Technology University, Wuhan 430022, China.No affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article
Research Support, Non-U.S. Gov't

Language

chi

PubMed ID

12890349

Citation

Wu, He-shui, et al. "[TLR4 Is Involved in Hepatic Ischemia/reperfusion Injury in Mice]." Zhonghua Gan Zang Bing Za Zhi = Zhonghua Ganzangbing Zazhi = Chinese Journal of Hepatology, vol. 11, no. 7, 2003, pp. 424-6.
Wu HS, Wang L, Rotstein O. [TLR4 is involved in hepatic ischemia/reperfusion injury in mice]. Zhonghua Gan Zang Bing Za Zhi. 2003;11(7):424-6.
Wu, H. S., Wang, L., & Rotstein, O. (2003). [TLR4 is involved in hepatic ischemia/reperfusion injury in mice]. Zhonghua Gan Zang Bing Za Zhi = Zhonghua Ganzangbing Zazhi = Chinese Journal of Hepatology, 11(7), 424-6.
Wu HS, Wang L, Rotstein O. [TLR4 Is Involved in Hepatic Ischemia/reperfusion Injury in Mice]. Zhonghua Gan Zang Bing Za Zhi. 2003;11(7):424-6. PubMed PMID: 12890349.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [TLR4 is involved in hepatic ischemia/reperfusion injury in mice]. AU - Wu,He-shui, AU - Wang,Lin, AU - Rotstein,Ori, PY - 2003/8/2/pubmed PY - 2004/1/7/medline PY - 2003/8/2/entrez SP - 424 EP - 6 JF - Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology JO - Zhonghua Gan Zang Bing Za Zhi VL - 11 IS - 7 N2 - OBJECTIVES: To explore the role of TLR4 in the mechanism of hepatic ischemia/reperfusion (I/R) injury in mice. METHODS: Wild-type (C3H/Heouj) mice and TLR4 deficient mice (C3H/Hej) were used to prepare the models of liver I/R injury. Partial hepatic ischemia was produced by inflow causing occlusion in the median and left lobes for 45 minutes. Blood was drawn to kill the mice at 1 hours and 3 hours after reperfusion. The blood was used to analyze aspartate aminotransferase (AST) and tumor necrosis factor-alpha (TNFalpha). TNF-alpha mRNA expression and myeloperoxidase (MPO) level in ischemic lobes was examined by northern blot and myeloperoxidase assay, respectively. RESULTS: AST levels were significantly lower in TLR4 deficient mice, compared with those in wild-type mice at both time points (661.83U/L+/-106.09U/L vs. 1215.5U/L+/- 174.03U/L, t=-6.65, P<0.01; 1145.17U/L+/-132.42U/L vs. 2958.17U/L+/-186.81U/L, t=-5.57, P<0.01). Serum TNF-alpha level was lower in TLR4 deficient mice at 3 hours after reperfusion compared with that in wild-type mice (152.39pg/ml+/-43.3 pg/ml vs. 249.12pg/ml+/-51.89pg/ml, t=-3.13, P<0.05). This difference appeared to be mediated at the gene level, since TNF-alpha mRNA expression had decreased in TLR4 deficient mice at 1 hours after reperfusion, compared with that in wild type mice (80.3+/-28.8 vs. 189.4+/-24.6, t=-3.25, P<0.05). MPO level in ischemic lobes in TLR4 deficient mice at 3 hours after reperfusion was significantly lower than that in wild type mice (F=33.49, P<0.01). CONCLUSIONS: I/R hepatic injury in TLR4 deficient mice is less than that in wild-type mice. TNF-alpha expression down-regulated at the mRNA level appears critical. These suggest that TLR4 be involved in the mechanism of hepatic ischemia/reperfusion injury in mice. SN - 1007-3418 UR - https://www.unboundmedicine.com/medline/citation/12890349/[TLR4_is_involved_in_hepatic_ischemia/reperfusion_injury_in_mice]_ DB - PRIME DP - Unbound Medicine ER -