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Rat Liver Ischemia/Reperfusion Induced Proinflammatory Mediator
Type
article
Resource
Transplantation Proceedings.(40):2156-2158.
Date Issued
2008
Author(s)
蘇千玲
Hsu Y.C.; Chou TY; Chen CF; Wang D; Su CL; Hu RT
Subjects
呼吸治療學系
期刊論文
Abstract
Objective. Ischemia/reperfusion (I/R) of the rat liver induces injury; however, few
studies have investigated gene expressions associated with this phenomenon. In this study,
gene chip and real-time polymerase chain reactions (PCR) were used to study the
expressions of the proinflammatory mediators and antioxidants after I/R.
Materials and Methods. Ischemia was induced by clamping the common hepatic artery
and portal vein for 40 minutes followed by 90 minutes reperfusion. Blood samples
collected before ischemia and after reperfusion were analyzed for alanine amino transferase,
lactic dehydrogenase, hydroxyl radicals, nitric oxide (NO), and tumor necrosis
factor (TNF). Expressions of TNF, interleukin 12 (IL12), cyclooxygenase II (COXII),
and other inflammatory mediators were analyzed by gene chips. COXII, TNF, and
antioxidants of mitochondrial superoxide dismutase (SOD(Mn)), catalase, and heat shock
protein 70 (HSP70) were double confirmed by real-time PCRs.
Results. This protocol resulted in elevations in the blood concentrations of NO, hydroxyl
radicals, TNF, ALT, and LDH (P .01) in the I/R but not the sham-operated group.
Reperfusion induced significant increases in the expressions of TNF, IL12, COXII,
SOD(Mn), catalase, and HSP70. Real-time PCR also demonstrated increases in mRNA
expressions of the proinflammatory mediators and antioxidants.
Conclusions. This protocol resulted in oxidative stress, nitrosative stress, and liver
injury. The increases in expressions of both proinflammatory mediators and antioxidants
suggested that an imbalance between inflammation and anti-inflammation could be the
possible reason for the liver injury after I/R.
studies have investigated gene expressions associated with this phenomenon. In this study,
gene chip and real-time polymerase chain reactions (PCR) were used to study the
expressions of the proinflammatory mediators and antioxidants after I/R.
Materials and Methods. Ischemia was induced by clamping the common hepatic artery
and portal vein for 40 minutes followed by 90 minutes reperfusion. Blood samples
collected before ischemia and after reperfusion were analyzed for alanine amino transferase,
lactic dehydrogenase, hydroxyl radicals, nitric oxide (NO), and tumor necrosis
factor (TNF). Expressions of TNF, interleukin 12 (IL12), cyclooxygenase II (COXII),
and other inflammatory mediators were analyzed by gene chips. COXII, TNF, and
antioxidants of mitochondrial superoxide dismutase (SOD(Mn)), catalase, and heat shock
protein 70 (HSP70) were double confirmed by real-time PCRs.
Results. This protocol resulted in elevations in the blood concentrations of NO, hydroxyl
radicals, TNF, ALT, and LDH (P .01) in the I/R but not the sham-operated group.
Reperfusion induced significant increases in the expressions of TNF, IL12, COXII,
SOD(Mn), catalase, and HSP70. Real-time PCR also demonstrated increases in mRNA
expressions of the proinflammatory mediators and antioxidants.
Conclusions. This protocol resulted in oxidative stress, nitrosative stress, and liver
injury. The increases in expressions of both proinflammatory mediators and antioxidants
suggested that an imbalance between inflammation and anti-inflammation could be the
possible reason for the liver injury after I/R.
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