Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2017 Mar;9(3):702-710.
doi: 10.21037/jtd.2017.02.80.

Protective effect of propofol preconditioning on ischemia-reperfusion injury in human hepatocyte

Affiliations

Protective effect of propofol preconditioning on ischemia-reperfusion injury in human hepatocyte

Yuzhu Zhang et al. J Thorac Dis. 2017 Mar.

Abstract

Background: Blood reperfusion after ischemia is the main measure to restore cell function. This study was aimed to explore the effect of propofol on rat and cell models of liver ischemia-reperfusion (I/R) injury, and to investigate its possible mechanism.

Methods: Wistar rats were divided into four groups: control group, sham group, I/R group, and propofol group. Human hepatocyte HL7702 was divided into six groups: control group, I/R group and propofol (5, 10, 20 and 40 µmol/L) groups. After the animal and cell models were established, the alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA) and adenosine triphosphate (ATP) levels in liver tissues and hepatocytes were measured. Cell viability and apoptosis of hepatocytes were respectively determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry. Furthermore, the expressions of apoptosis-related proteins in hepatocytes were determined by Western blot analysis.

Results: ALT, AST and MDA levels were all decreased significantly, and the ATP level was increased significantly in propofol group compared with that in I/R group in both liver tissues and hepatocytes. Additionally, cell viability of hepatocytes in propofol group was higher than that in I/R group, while the percentage of apoptotic cells in propofol group was less than that in I/R group. Moreover, the expression of caspase-3 decreased and the expression of Bcl-2 increased significantly after propofol preconditioning.

Conclusions: Our findings suggested that propofol preconditioning might be an effective strategy for protecting the liver from I/R injury, which might provide a scientific basis for clinical application.

Keywords: Propofol; apoptosis; cell viability; hepatocyte; liver ischemia-reperfusion injury (liver I/R injury).

PubMed Disclaimer

Conflict of interest statement

Conflicts of Interest: The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
The ALT (A), AST (B), MDA (C) and ATP (D) levels in liver tissues in four groups. Data were presented as mean ± SD (**P<0.01). The significance of I/R group was compared with control/sham group while the significance of propofol group was compared with I/R group. ALT, alanine aminotransferase; AST, aspartate aminotransferase; MDA, malondialdehyde; ATP, adenosine triphosphate; I/R, ischemia-reperfusion.
Figure 2
Figure 2
The ALT (A), AST (B), MDA (C) and ATP (D) levels in human hepatocytes in six groups. Data were presented as mean ± SD (*, P<0.05; **, P<0.01; ***, P<0.001). The significance of I/R group was compared with control group while the significance of propofol groups were compared with I/R group. ALT, alanine aminotransferase; AST, aspartate aminotransferase; MDA, malondialdehyde; ATP, adenosine triphosphate; I/R, ischemia-reperfusion.
Figure 3
Figure 3
Cell viability of human hepatocytes assayed by MTT assay. Data were presented as mean ± SD (*P<0.05; **P<0.01). The significance of I/R group was compared with control group while the significance of propofol group was compared with I/R group. I/R, ischemia-reperfusion; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide.
Figure 4
Figure 4
Cell apoptosis of human hepatocytes. (A) The percentage of apoptotic cells assayed by flow cytometer; (B) the expressions of apoptosis-related proteins (caspase-3 and Bcl-2) in hepatocytes determined by Western blot analysis. Data were presented as mean ± SD (*, P<0.05). The significance on the top of the column was compared with control group. I/R, ischemia-reperfusion; Bcl-2, mammalian B cell lymphoma-2.

Similar articles

Cited by

References

    1. Baykara B, Tekmen I, Pekcetin C, et al. The protective effects of carnosine and melatonin in ischemia-reperfusion injury in the rat liver. Acta Histochemica 2009;111:42-51. 10.1016/j.acthis.2008.03.002 - DOI - PubMed
    1. Collard CD, Gelman S. Pathophysiology, clinical manifestations, and prevention of ischemia-reperfusion injury. Anesthesiology 2001;94:1133. 10.1097/00000542-200106000-00030 - DOI - PubMed
    1. Kaszaki J, Wolfárd A, Szalay L, et al. Pathophysiology of Ischemia-Reperfusion Injury. Transplant Proc 2006;38:826-8. 10.1016/j.transproceed.2006.02.152 - DOI - PubMed
    1. Cardinal J, Pan P, Tsung A. Protective role of cisplatin in ischemic liver injury through induction of autophagy. Autophagy 2009;5:1211-2. 10.4161/auto.5.8.9972 - DOI - PubMed
    1. Arii S, Teramoto K, Kawamura T. Current progress in the understanding of and therapeutic strategies for ischemia and reperfusion injury of the liver. J Hepatobiliary Pancreat Surg 2003;10:189-94. 10.1007/s00534-002-0720-z - DOI - PubMed