TY - JOUR
T1 - Oral administration of cilostazol improves survival rate after rat liver ischemia/reperfusion injury
AU - Fujii, Taku
AU - Obara, Hideaki
AU - Matsubara, Kentaro
AU - Fujimura, Naoki
AU - Yagi, Hiroshi
AU - Hibi, Taizo
AU - Abe, Yuta
AU - Kitago, Minoru
AU - Shinoda, Masahiro
AU - Itano, Osamu
AU - Tanabe, Minoru
AU - Masugi, Yohei
AU - Sakamoto, Michiie
AU - Kitagawa, Yuko
N1 - Funding Information:
Funding: This study was supported in part by Grant-in-Aid for Scientific Research (grant number 15k10172) of the Japan Society for the Promotion of Science (Tokyo, Japan).
Publisher Copyright:
© 2017 Elsevier Inc.
PY - 2017/6/1
Y1 - 2017/6/1
N2 - Background Cilostazol is a type III phosphodiesterase inhibitor used to treat the symptoms of intermittent claudication. Recent studies have shown that cilostazol decreases ischemia/reperfusion (I/R) injury in several organs. Materials and methods We evaluated the effects of cilostazol in a rat model of liver I/R injury. Thirty male Wistar rats with liver I/R injury were divided into a cilostazol or saline (control) group (n = 15 each). Each rat was orally administered cilostazol or saline for 3 d before I/R injury. Liver I/R injury was induced via 1 h of warm ischemia of the median and left lateral liver lobes, followed by 3 h of reperfusion. The rats were then euthanized. Serum aspartate aminotransferase, alanine aminotransferase, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α levels were measured. The Mann–Whitney U test was used to compare the differences between the treatment groups. Histologic examination was performed on the liver tissues. We also conducted a survival study to confirm the effect of cilostazol on the mortality rate in rats. For the survival study, a liver I/R injury model with an ischemia time of 1.5 h was used, and the rats were observed for 1 wk. Results Serum aspartate aminotransferase, alanine aminotransferase, IL-1β, and IL-6 levels were significantly lower in the cilostazol group than in the saline group. Treatment with cilostazol significantly improved pathological findings associated with liver I/R injury and increased survival rate compared to that in controls. Conclusions Cilostazol reduced mortality and alleviated the effects of liver I/R injury in Wistar rats.
AB - Background Cilostazol is a type III phosphodiesterase inhibitor used to treat the symptoms of intermittent claudication. Recent studies have shown that cilostazol decreases ischemia/reperfusion (I/R) injury in several organs. Materials and methods We evaluated the effects of cilostazol in a rat model of liver I/R injury. Thirty male Wistar rats with liver I/R injury were divided into a cilostazol or saline (control) group (n = 15 each). Each rat was orally administered cilostazol or saline for 3 d before I/R injury. Liver I/R injury was induced via 1 h of warm ischemia of the median and left lateral liver lobes, followed by 3 h of reperfusion. The rats were then euthanized. Serum aspartate aminotransferase, alanine aminotransferase, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α levels were measured. The Mann–Whitney U test was used to compare the differences between the treatment groups. Histologic examination was performed on the liver tissues. We also conducted a survival study to confirm the effect of cilostazol on the mortality rate in rats. For the survival study, a liver I/R injury model with an ischemia time of 1.5 h was used, and the rats were observed for 1 wk. Results Serum aspartate aminotransferase, alanine aminotransferase, IL-1β, and IL-6 levels were significantly lower in the cilostazol group than in the saline group. Treatment with cilostazol significantly improved pathological findings associated with liver I/R injury and increased survival rate compared to that in controls. Conclusions Cilostazol reduced mortality and alleviated the effects of liver I/R injury in Wistar rats.
KW - Alanine aminotransferase
KW - Aspartate aminotransferase
KW - Cilostazol
KW - Hepatocyte injury
KW - Partial ischemia/reperfusion injury
KW - Phosphodiesterase III inhibitor
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U2 - 10.1016/j.jss.2017.02.020
DO - 10.1016/j.jss.2017.02.020
M3 - Article
C2 - 28601316
AN - SCOPUS:85015862189
SN - 0022-4804
VL - 213
SP - 207
EP - 214
JO - Journal of Surgical Research
JF - Journal of Surgical Research
ER -