Oxidative stress induced by portal vein embolization in fatty liver: Experimental study of a nonalcoholic steatohepatitis model

Baba,Yasutaka; Hayashi,Sadao; Nagasato,Kohei; Higashi,Michiyo; Tosuji,Nanako; Sonoda,Shunro; Yoshiura,Takashi

doi:10.3892/br.2018.1141

Oxidative stress induced by portal vein embolization in fatty liver: Experimental study of a nonalcoholic steatohepatitis model

Authors:
- Yasutaka Baba
- Sadao Hayashi
- Kohei Nagasato
- Michiyo Higashi
- Nanako Tosuji
- Shunro Sonoda
- Takashi Yoshiura
View Affiliations

Affiliations: Department of Radiology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima 890-8544, Japan, Department of Human Pathology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima 890-8544, Japan, Department of International Island and Community Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima 890-8544, Japan
Published online on: August 8, 2018 https://doi.org/10.3892/br.2018.1141
Pages: 357-363

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )

Metrics: Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )

Cited By (CrossRef): 0 citations Loading Articles...

Abstract

The present study aimed to investigate whether excessive oxidative stress production or reduction of antioxidative stress potential may occur following portal vein embolization (PVE) in an experimental animal nonalcoholic steatohepatitis (NASH) model. A NASH rabbit model (n=11) was established by feeding of a fat diet for 4 weeks, and a normal diet rabbit model (n=11) was prepared as a control. The oxidative status of NASH was examined by measuring derivatives of reactive oxygen metabolites (d-ROM) for oxidative stress and biological antioxidative potential (BAP) for antioxidative potential in the NASH model and normal group. Additionally, oxidative status of PVE after 2 weeks was assessed by measuring d-ROM and BAP in the NASH and normal liver models. Oxidative status in a PVE+NASH model was also detected. In the process of NASH creation (fat diet for 4 weeks), total cholesterol was increased in the NASH group (P<0.0001). In the NASH group, PVE induced an increase in serum aspartate transaminase (P=0.0318). At 4 weeks after initiation of the fat diet, a decrease in BAP was determined as statistically significant (P<0.0001). In normal liver, d-ROM production was stimulated in the Sham group after 2 weeks (P=0.0152), but BAP was not altered (P=0.6119). In NASH liver, d-ROM production was stimulated in PVE and Sham groups (P<0.0001 and P=0.0189, respectively), but BAP did not change (P>0.05). In conclusion, decrease of antioxidant potential may promote NASH progression. Additionally, PVE appeared to cause a surge in oxidative stress in NASH liver.

View Figures

View References

1	Baba Y, Sonoda JI, Hayashi S, Tosuji N, Sonoda S, Makisumi K and Nakajo M: Reduction of oxidative stress in liver cancer patients by oral green tea polyphenol tablets during hepatic arterial infusion chemotherapy. Exp Ther Med. 4:452–458. 2012. View Article : Google Scholar : PubMed/NCBI
2	Yokoyama Y, Nagino M and Nimura Y: Mechanisms of hepatic regeneration following portal vein embolization and partial hepatectomy: A review. World J Surg. 31:367–374. 2007. View Article : Google Scholar : PubMed/NCBI
3	Khan AZ, Morris-Stiff G and Makuuchi M: Patterns of chemotherapy-induced hepatic injury and their implications for patients undergoing liver resection for colorectal liver metastases. J Hepatobiliary Pancreat Surg. 16:137–144. 2009. View Article : Google Scholar : PubMed/NCBI
4	Narita M, Oussoultzoglou E, Chenard MP, Rosso E, Casnedi S, Pessaux P, Bachellier P and Jaeck D: Sinusoidal obstruction syndrome compromises liver regeneration in patients undergoing two-stage hepatectomy with portal vein embolization. Surg Today. 41:7–17. 2011. View Article : Google Scholar : PubMed/NCBI
5	Usuki N: Selective segmental necrotizing therapy for hepatocellular carcinoma: An experimental study of an ethanol injection method. Nihon Igaku Hoshasen Gakkai Zasshi. 54:1142–1154. 1994.(In Japanese). PubMed/NCBI
6	Fu JF, Fang YL, Liang L, Wang CL, Hong F and Dong GP: A rabbit model of pediatric nonalcoholic steatohepatitis: The role of adiponectin. World J Gastroenterol. 15:912–918. 2009. View Article : Google Scholar : PubMed/NCBI
7	Brunt EM, Janney CG, Di Bisceglie AM, Neuschwander-Tetri BA and Bacon BR: Nonalcoholic steatohepatitis: A proposal for grading and staging the histological lesions. Am J Gastroenterol. 94:2467–2474. 1999. View Article : Google Scholar : PubMed/NCBI
8	Sutti S, Jindal A, Locatelli I, Vacchiano M, Gigliotti L, Bozzola C and Albano E: Adaptive immune responses triggered by oxidative stress contribute to hepatic inflammation in NASH. Hepatology. 59:886–897. 2014. View Article : Google Scholar : PubMed/NCBI
9	Ypsilantis P, Lambropoulou M, Anagnostopoulos C, Tentes I, Tsigalou C, Pitiakoudis M, Kortsaris A, Papadopoulos N and Simopoulos C: Mesna preserves hepatocyte regenerating capacity following liver radiofrequency ablation under Pringle maneuver. J Surg Res. 169:44–50. 2011. View Article : Google Scholar : PubMed/NCBI
10	Handa P, Morgan-Stevenson V, Maliken BD, Nelson JE, Washington S, Westerman M, Yeh MM and Kowdley KV: Iron overload results in hepatic oxidative stress, immune cell activation, and hepatocellular ballooning injury, leading to nonalcoholic steatohepatitis in genetically obese mice. Am J Physiol Gastrointest Liver Physiol. 310:G117–G127. 2016. View Article : Google Scholar : PubMed/NCBI
11	Furukawa S, Fujita T, Shimabukuro M, Iwaki M, Yamada Y, Nakajima Y, Nakayama O, Makishima M, Matsuda M and Shimomura I: Increased oxidative stress in obesity and its impact on metabolic syndrome. J Clin Invest. 114:1752–1761. 2004. View Article : Google Scholar : PubMed/NCBI
12	Vecchione G, Grasselli E, Compalati AD, Ragazzoni M, Cortese K, Gallo G, Voci A and Vergani L: Ethanol and fatty acids impair lipid homeostasis in an in vitro model of hepatic steatosis. Food Chem Toxicol. 90:84–94. 2016. View Article : Google Scholar : PubMed/NCBI
13	Liu W, Baker RD, Bhatia T, Zhu L and Baker SS: Pathogenesis of nonalcoholic steatohepatitis. Cell Mol Life Sci. 73:1969–1987. 2016. View Article : Google Scholar : PubMed/NCBI
14	Li S, Zeng XY, Zhou X, Wang H, Jo E, Robinson SR, Xu A and Ye JM: Dietary cholesterol induces hepatic inflammation and blunts mitochondrial function in the liver of high-fat-fed mice. J Nutr Biochem. 27:96–103. 2016. View Article : Google Scholar : PubMed/NCBI
15	Kitade H, Chen G, Ni Y and Ota T: Nonalcoholic fatty liver disease and insulin resistance: New insights and potential new treatments. Nutrients. 9:E3872017. View Article : Google Scholar : PubMed/NCBI
16	Richter K and Kietzmann T: Reactive oxygen species and fibrosis: Further evidence of a significant liaison. Cell Tissue Res. 365:591–605. 2016. View Article : Google Scholar : PubMed/NCBI