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. 2018 Jan 8:2018:3812424.
doi: 10.1155/2018/3812424. eCollection 2018.

Prostaglandin E1 Preconditioning Attenuates Liver Ischemia Reperfusion Injury in a Rat Model of Extrahepatic Cholestasis

Feng Xu  1 , Xiaolin Liu  1 , Chao Wang  1 , Chaoliu Dai  1
Affiliations

Prostaglandin E1 Preconditioning Attenuates Liver Ischemia Reperfusion Injury in a Rat Model of Extrahepatic Cholestasis

Feng Xu et al. Biomed Res Int. .

Abstract

The aim of this study is to explore the hepatoprotective effect of intraportal prostaglandin E1 (PGE1) on liver ischemia reperfusion (IR) injury using an extrahepatic cholestatic model, observing oxidative stress markers, proinflammatory factors, apoptotic marker proteins, and an adhesion molecule. The extrahepatic cholestatic model was induced by common bile duct ligation. After seven days, rats were subjected to ischemia by Pringle maneuver for 15 min, followed by 1, 6, or 24 h of reperfusion. Prostaglandin E1 (PGE group) or normal saline (NS group) was continuously infused from 15 min before liver ischemia to 1 h after reperfusion. After reperfusion, histopathological evaluation of the liver was performed, as were measurements of bilirubin, biochemical enzymes, oxidative stress markers (GSH and MDA), proinflammatory factors (MPO, TNF-α, and IL-1β), apoptotic marker proteins (Bcl-2 and Bax), and the adhesion molecule (ICAM-1). PGE1 pretreatment attenuated IR injury in extrahepatic cholestatic liver probably by suppressing MDA, MPO, TNF-α, IL-1β, ICAM-1, and Bax levels and improving GSH and Bcl-2 levels. In conclusion, PGE1 protects extrahepatic cholestatic liver from IR injury by improving hepatic microcirculation and reducing oxidative stress damage, intrahepatic neutrophil infiltration, and hepatocyte apoptosis.

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Figures

Figure 1
Figure 1
The serum levels of bilirubin (μmol/L) and biochemical enzymes (ALP, ALT, AST, and LDH) (U/L) in PGE group and NS group at 1, 6, and 24 h after reperfusion. The data are expressed as the mean ± SD (n = 6, ∗P < 0.05, and ∗∗P < 0.001).
Figure 2
Figure 2
Histopathological changes in the liver tissue of each group at 1, 6, and 24 h after reperfusion. Representative hematoxylin-and-eosin (HE) stained microphotographs were taken from the NS group (a, c, and e) and the PGE group (b, d, and f) (original magnification, ×400). (g) Suzuki's score: the data are expressed as the mean ± SD (n = 6, ∗P < 0.05, ∗∗P < 0.001, and ∗∗∗P < 0.0001).
Figure 3
Figure 3
The levels of GSH and MDA in liver tissue in PGE group and NS group at 1, 6, and 24 h after reperfusion. The data are expressed as the mean ± SD (n = 6, ∗P < 0.05, and ∗∗P < 0.001).
Figure 4
Figure 4
The expression of ICAM-1 in liver tissue of PGE group and NS group at 1, 6, and 24 h after reperfusion as measured by immunohistochemical staining (a–f, magnification, ×400). The average integral optical density (IOD) of ICAM-1 expression in the two groups: the data are expressed as the mean ± SD (n = 6, ∗P < 0.05, and ∗∗∗P < 0.0001).
Figure 5
Figure 5
The levels of MPO, IL-1β, and TNF-α in liver tissue in PGE group and NS group at 1, 6, and 24 h after reperfusion. The data are expressed as the mean ± SD (n = 6, ∗P < 0.05, and ∗∗P < 0.001).
Figure 6
Figure 6
The expressions of Bcl-2 in liver tissue of PGE group and NS group at 1, 6, and 24 h after reperfusion as measured by immunohistochemical staining (a–f, magnification, ×400). The average integral optical density (IOD) of Bcl-2 expression in two groups: the data are expressed as the mean ± SD (n = 6, ∗P < 0.05, and ∗∗P < 0.001).
Figure 7
Figure 7
The expression of Bax in liver tissues of the PGE and NS groups at 1, 6, and 24 h after reperfusion as measured by immunohistochemical staining (a–f, magnification, ×400). (g) The average integral optical density (IOD) of Bax expression in two groups: the data are expressed as the mean ± SD (n = 6, ∗P < 0.05).
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