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Liver tissue inducible nitric oxide synthase (iNOS) expression and lipid peroxidation in experimental hepatic ischemia reperfusion injury stimulated with lipopolysaccharide: the role of aminoguanidine.
J Surg Res. 2008 Aug; 148(2):214-23.JS

Abstract

BACKGROUND

Hepatic ischemia-reperfusion (HIR) is a severe condition that is seen after hepatic arterial injury and in hepatic grafts in living donor transplantation. HIR not only causes liver injury by lipid peroxidation, but also stimulates systemic and portal endotoxemia. Also, lipopolysaccharide (LPS) induces hepatic injury mediated by inducible nitric oxide synthase (iNOS). There is little knowledge on the role of specific iNOS inhibitors in prevention of HIR injury followed by LPS administration. The aim of this study on a LPS induced HIR model was to investigate the effect of aminoguanidine (AG) administration on hepatic tissue iNOS expression and lipid peroxidation when given before or after LPS.

METHODS

Six groups were designed; A: Sham, B: HIR, C: HIR + AG, D: HIR + LPS, E: HIR + LPS + AG, F: HIR + AG + LPS. No substance was given to the rats in Group A and B. HIR injury was induced with vascular occlusion for 45 min and reperfusion for 45 min. Drugs were given intraperitoneally 10 min before reperfusion. Serum and tissue analysis for myeloperoxidase (MPO), and malondialdehyde (MDA), and tissue NA+/K+ adenosine 5'triphosphatases (ATPase) and tissue iNOS staining were performed. Permission for this study was obtained from the local Ethics Committee.

RESULTS

The level of MPO, MDA, and iNOS staining scores in Group B were significantly higher than Group A and ATPase was lower in Group B (P < 0.05). Contrary to results in Group C, results of MPO, MDA, and iNOS staining scores of Group D was higher than Group B (P < 0.05); however, although iNOS in Group C was lower than Group B, the difference was not significant (P > 0.05). MPO and MDA levels of Groups E and F were significantly lower than Group D. Level of ATPase in Group F was significantly different from Groups D and E. iNOS scoring was low in Group F compared with Group D (P < 0.05). MDA, MPO, and iNOS levels of Group F was lower than Group E, and ATPase of Group F was higher than Group E (P < 0.05).

CONCLUSIONS

The results of this study in a LPS induced HIR model showed that LPS after HIR aggravated HIR injury by increasing neutrophil activation and lipid peroxidation both in serum and liver tissue and iNOS in liver, and depleting energy in liver. AG, a selective iNOS inhibitor, ameliorated the negative effects of endotoxemia induced by LPS after HIR; however, energy depletion and iNOS expression in liver tissue were attenuated only when AG was administered prior to LPS. The findings of this study supported the hypothesis that LPS after HIR would aggravate HIR injury and AG would ameliorate this aggravated injury.

Authors+Show Affiliations

Department of General Surgery, Dumlupinar University Hospital, Kutahya, Turkey. faikyaylak@lycos.comNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18222473

Citation

Yaylak, Faik, et al. "Liver Tissue Inducible Nitric Oxide Synthase (iNOS) Expression and Lipid Peroxidation in Experimental Hepatic Ischemia Reperfusion Injury Stimulated With Lipopolysaccharide: the Role of Aminoguanidine." The Journal of Surgical Research, vol. 148, no. 2, 2008, pp. 214-23.
Yaylak F, Canbaz H, Caglikulekci M, et al. Liver tissue inducible nitric oxide synthase (iNOS) expression and lipid peroxidation in experimental hepatic ischemia reperfusion injury stimulated with lipopolysaccharide: the role of aminoguanidine. J Surg Res. 2008;148(2):214-23.
Yaylak, F., Canbaz, H., Caglikulekci, M., Dirlik, M., Tamer, L., Ogetman, Z., Polat, Y., Kanik, A., & Aydin, S. (2008). Liver tissue inducible nitric oxide synthase (iNOS) expression and lipid peroxidation in experimental hepatic ischemia reperfusion injury stimulated with lipopolysaccharide: the role of aminoguanidine. The Journal of Surgical Research, 148(2), 214-23. https://doi.org/10.1016/j.jss.2007.10.008
Yaylak F, et al. Liver Tissue Inducible Nitric Oxide Synthase (iNOS) Expression and Lipid Peroxidation in Experimental Hepatic Ischemia Reperfusion Injury Stimulated With Lipopolysaccharide: the Role of Aminoguanidine. J Surg Res. 2008;148(2):214-23. PubMed PMID: 18222473.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Liver tissue inducible nitric oxide synthase (iNOS) expression and lipid peroxidation in experimental hepatic ischemia reperfusion injury stimulated with lipopolysaccharide: the role of aminoguanidine. AU - Yaylak,Faik, AU - Canbaz,Hakan, AU - Caglikulekci,Mehmet, AU - Dirlik,Musa, AU - Tamer,Lulufer, AU - Ogetman,Zekai, AU - Polat,Yalcin, AU - Kanik,Arzu, AU - Aydin,Süha, Y1 - 2007/11/26/ PY - 2007/05/23/received PY - 2007/09/14/revised PY - 2007/10/12/accepted PY - 2008/1/29/pubmed PY - 2008/8/20/medline PY - 2008/1/29/entrez SP - 214 EP - 23 JF - The Journal of surgical research JO - J Surg Res VL - 148 IS - 2 N2 - BACKGROUND: Hepatic ischemia-reperfusion (HIR) is a severe condition that is seen after hepatic arterial injury and in hepatic grafts in living donor transplantation. HIR not only causes liver injury by lipid peroxidation, but also stimulates systemic and portal endotoxemia. Also, lipopolysaccharide (LPS) induces hepatic injury mediated by inducible nitric oxide synthase (iNOS). There is little knowledge on the role of specific iNOS inhibitors in prevention of HIR injury followed by LPS administration. The aim of this study on a LPS induced HIR model was to investigate the effect of aminoguanidine (AG) administration on hepatic tissue iNOS expression and lipid peroxidation when given before or after LPS. METHODS: Six groups were designed; A: Sham, B: HIR, C: HIR + AG, D: HIR + LPS, E: HIR + LPS + AG, F: HIR + AG + LPS. No substance was given to the rats in Group A and B. HIR injury was induced with vascular occlusion for 45 min and reperfusion for 45 min. Drugs were given intraperitoneally 10 min before reperfusion. Serum and tissue analysis for myeloperoxidase (MPO), and malondialdehyde (MDA), and tissue NA+/K+ adenosine 5'triphosphatases (ATPase) and tissue iNOS staining were performed. Permission for this study was obtained from the local Ethics Committee. RESULTS: The level of MPO, MDA, and iNOS staining scores in Group B were significantly higher than Group A and ATPase was lower in Group B (P < 0.05). Contrary to results in Group C, results of MPO, MDA, and iNOS staining scores of Group D was higher than Group B (P < 0.05); however, although iNOS in Group C was lower than Group B, the difference was not significant (P > 0.05). MPO and MDA levels of Groups E and F were significantly lower than Group D. Level of ATPase in Group F was significantly different from Groups D and E. iNOS scoring was low in Group F compared with Group D (P < 0.05). MDA, MPO, and iNOS levels of Group F was lower than Group E, and ATPase of Group F was higher than Group E (P < 0.05). CONCLUSIONS: The results of this study in a LPS induced HIR model showed that LPS after HIR aggravated HIR injury by increasing neutrophil activation and lipid peroxidation both in serum and liver tissue and iNOS in liver, and depleting energy in liver. AG, a selective iNOS inhibitor, ameliorated the negative effects of endotoxemia induced by LPS after HIR; however, energy depletion and iNOS expression in liver tissue were attenuated only when AG was administered prior to LPS. The findings of this study supported the hypothesis that LPS after HIR would aggravate HIR injury and AG would ameliorate this aggravated injury. SN - 1095-8673 UR - https://www.unboundmedicine.com/medline/citation/18222473/Liver_tissue_inducible_nitric_oxide_synthase__iNOS__expression_and_lipid_peroxidation_in_experimental_hepatic_ischemia_reperfusion_injury_stimulated_with_lipopolysaccharide:_the_role_of_aminoguanidine_ DB - PRIME DP - Unbound Medicine ER -