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. 2018 Dec;16(6):5227-5235.
doi: 10.3892/etm.2018.6835. Epub 2018 Oct 9.

Significance of malondialdehyde, superoxide dismutase and endotoxin levels in Budd-Chiari syndrome in patients and a rat model

De-Lei Cheng  1   2 , Nan Zhu  3 , Cheng-Li Li  1 , Wei-Fu Lv  2 , Wei-Wei Fang  2 , Ya Liu  4 , Chuan-Ting Li  1
Affiliations

Significance of malondialdehyde, superoxide dismutase and endotoxin levels in Budd-Chiari syndrome in patients and a rat model

De-Lei Cheng et al. Exp Ther Med. 2018 Dec.

Abstract

Budd-Chiari syndrome (BCS) is a rare clinical syndrome caused by the obstruction of hepatic venous outflow. In theory, hepatic congestion and hypoxia induce pathological damage and changes in the liver. However, at present, laboratory evidence supporting this theory is lacking. The aim of the present study was to assess the expression and significance of the hypoxia-associated indicators malondialdehyde (MDA), superoxide dismutase (SOD) and endotoxin (ET) in the liver and serum of subjects with BCS. An animal model of BCS was established by partial ligation of the inferior vena cava (IVC) in rats. The levels of MDA, SOD and ET in the serum of BCS patients, as well as in the liver and serum of rats with BCS, were detected and analyzed. In human patients with BCS, the serum levels of MDA, ET and SOD were significantly different from those in healthy control subjects. In the animal model, similar trends were observed regarding the MDA, ET and SOD levels in liver homogenate and serum (P<0.05), the degree of which was more pronounced in the liver homogenate than in the serum. At 6 weeks after the surgery, these indicators reached peak/valley levels in the experimental group and were at least partially restored by week 12. A negative correlation between MDA and SOD, a positive correlation between MDA and ET, and a negative correlation between SOD and ET was identified. In conclusion, the levels of hypoxia-associated indicators significantly changed with BCS progression, suggesting that hypoxia is a major factor in the pathogenesis of BCS.

Keywords: Budd-Chiari syndrome; endotoxin; hypoxia; reactive oxygen species.

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Figures

Figure 1.
Figure 1.
Flow chart illustrating the animal experiment and grouping. IVC, inferior vena cava; SD, Sprague Dawley.
Figure 2.
Figure 2.
Hypoxia indicators in human patients. *P<0.001 vs. Patient group. MDA, malondialdehyde; SOD, superoxide dismutase; ET, endotoxin.
Figure 3.
Figure 3.
(A) Digital subtraction angiography indicated that the lumen of the inferior vena cava in the posterior segment of the liver from an experimental rat was significantly narrowed (red arrow) and the distal lumen was dilated with collateral circulation (blue arrow). (B) Hematoxylin and eosin staining revealed pathological changes in the liver from an experimental rat (magnification, ×400): Abnormal arrangement of the hepatocyte cord, widened hepatic sinusoids (blue arrow) and a large number of red blood cells in the hepatic sinusoid (yellow arrow).
Figure 4.
Figure 4.
(A) MDA, (B) SOD and (C) ET levels in the liver homogenate and serum of the control and the experimental animal group at various time-points. MDA and ET increased post-operatively prior to reaching a peak by 6 weeks and decreasing slightly by 12 weeks. SOD decreased post-operatively prior to reaching a peak by 6 weeks and increasing slightly by 12 weeks. Groups: 1, control group; 2–5, experimental subgroup at 1, 3, 6 and 12 weeks, respectively. aP<0.05 vs. 1 week experiment group; bP<0.05 vs. 3 weeks experiment group; cP<0.05 vs. 6 weeks experiment group; dP<0.05 vs. 12 weeks experiment group; MDA, malondialdehyde; SOD, superoxide dismutase; ET, endotoxin.
Figure 5.
Figure 5.
Changes in (A) MDA, (B) SOD and (C) ET levels over time in liver homogenate and serum. The changes in the levels were expressed as the experimental subgroup/sham subgroup ×100% at each time-point. MDA, malondialdehyde; SOD, superoxide dismutase; ET, endotoxin.
Figure 6.
Figure 6.
Correlations between MDA, SOD and ET levels in liver homogenate and serum. MDA, malondialdehyde; SOD, superoxide dismutase; ET, endotoxin.
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