Abstract
Background/Aims: The role of uncoupling protein-2 (UCP2) in the liver is currently unclear. Emerging evidence suggests a relationship between UCP2 and oxidative stress. In the present study, we tested the hypothesis that UCP2 expression in the liver might change during warm ischemia-reperfusion (I/R) according to oxidative stress. Methods: Wistar rats were subjected to 40 (short ischemia) or 90 (long ischemia) minutes of partial lobar ischemia followed by 4 hours of reperfusion. UCP2 expression in the ischemic and nonischemic lobes was assessed using reverse transcription-polymerase chain reaction and immunohistochemistry. Malondialdehyde concentrations in the liver tissue were also compared. Results: Malondialdehyde concentrations in the ischemic lobes were significantly higher in the long ischemia group. In the ischemic lobes of the short ischemia group, UCP2 protein expression was induced in hepatocytes, which did not express the protein prior to treatment, and the expression levels were higher than in the long ischemia group. The intralobular distribution of UCP2 seemed to correlate inversely with that of the necrotic area. UCP2 expression was observed, even in nonischemic lobes with similar intralobular heterogeneity. Conclusions: UCP2 was induced in hepatocytes after warm I/R. Although the primitive role of UCP2 expression may be cytoprotective in nature, its actual protective effect in hepatic I/R may be minimal.
| Original language | English |
|---|---|
| Pages (from-to) | 486-492 |
| Number of pages | 7 |
| Journal | Gut and Liver |
| Volume | 5 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - Dec 1 2011 |
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All Science Journal Classification (ASJC) codes
- Hepatology
- Gastroenterology
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Role of UCP2 expression after hepatic warm ischemia-reperfusion in the rat. / Ninomiya, Mizuki; Shirabe, Ken; Shimada, Mitsuo; Terashi, Takahiro; Maehara, Yoshihiko.
In: Gut and Liver, Vol. 5, No. 4, 01.12.2011, p. 486-492.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Role of UCP2 expression after hepatic warm ischemia-reperfusion in the rat
AU - Ninomiya, Mizuki
AU - Shirabe, Ken
AU - Shimada, Mitsuo
AU - Terashi, Takahiro
AU - Maehara, Yoshihiko
PY - 2011/12/1
Y1 - 2011/12/1
N2 - Background/Aims: The role of uncoupling protein-2 (UCP2) in the liver is currently unclear. Emerging evidence suggests a relationship between UCP2 and oxidative stress. In the present study, we tested the hypothesis that UCP2 expression in the liver might change during warm ischemia-reperfusion (I/R) according to oxidative stress. Methods: Wistar rats were subjected to 40 (short ischemia) or 90 (long ischemia) minutes of partial lobar ischemia followed by 4 hours of reperfusion. UCP2 expression in the ischemic and nonischemic lobes was assessed using reverse transcription-polymerase chain reaction and immunohistochemistry. Malondialdehyde concentrations in the liver tissue were also compared. Results: Malondialdehyde concentrations in the ischemic lobes were significantly higher in the long ischemia group. In the ischemic lobes of the short ischemia group, UCP2 protein expression was induced in hepatocytes, which did not express the protein prior to treatment, and the expression levels were higher than in the long ischemia group. The intralobular distribution of UCP2 seemed to correlate inversely with that of the necrotic area. UCP2 expression was observed, even in nonischemic lobes with similar intralobular heterogeneity. Conclusions: UCP2 was induced in hepatocytes after warm I/R. Although the primitive role of UCP2 expression may be cytoprotective in nature, its actual protective effect in hepatic I/R may be minimal.
AB - Background/Aims: The role of uncoupling protein-2 (UCP2) in the liver is currently unclear. Emerging evidence suggests a relationship between UCP2 and oxidative stress. In the present study, we tested the hypothesis that UCP2 expression in the liver might change during warm ischemia-reperfusion (I/R) according to oxidative stress. Methods: Wistar rats were subjected to 40 (short ischemia) or 90 (long ischemia) minutes of partial lobar ischemia followed by 4 hours of reperfusion. UCP2 expression in the ischemic and nonischemic lobes was assessed using reverse transcription-polymerase chain reaction and immunohistochemistry. Malondialdehyde concentrations in the liver tissue were also compared. Results: Malondialdehyde concentrations in the ischemic lobes were significantly higher in the long ischemia group. In the ischemic lobes of the short ischemia group, UCP2 protein expression was induced in hepatocytes, which did not express the protein prior to treatment, and the expression levels were higher than in the long ischemia group. The intralobular distribution of UCP2 seemed to correlate inversely with that of the necrotic area. UCP2 expression was observed, even in nonischemic lobes with similar intralobular heterogeneity. Conclusions: UCP2 was induced in hepatocytes after warm I/R. Although the primitive role of UCP2 expression may be cytoprotective in nature, its actual protective effect in hepatic I/R may be minimal.
UR - http://www.scopus.com/inward/record.url?scp=81855220296&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=81855220296&partnerID=8YFLogxK
U2 - 10.5009/gnl.2011.5.4.486
DO - 10.5009/gnl.2011.5.4.486
M3 - Article
C2 - 22195248
AN - SCOPUS:81855220296
VL - 5
SP - 486
EP - 492
JO - Gut and Liver
JF - Gut and Liver
SN - 1976-2283
IS - 4
ER -