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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Inhibition of inducible nitric oxide synthase protects against the deleterious effects of sub-lethal sepsis and ethanol in the cardiorenal system

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Author(s):
Sousa, Arthur H. [1] ; do Vale, Gabriel T. [1, 2] ; Nascimento, Jose A. [1] ; Awata, Wanessa M. C. [3, 1] ; Silva, Carla B. P. [4, 1] ; Assis, Victor O. [1] ; Alves, V, Juliano ; Tostes, Rita C. [5] ; Tirapelli, Carlos R. [1]
Total Authors: 9
Affiliation:
[1] Univ Sao Paulo, DEPCH, Lab Farmacol, Escola Enfermagem Ribeirao Preto, Ribeirao Preto, SP - Brazil
[2] Univ Estado Minas Gerais UEMG, Belo Horizonte, MG - Brazil
[3] Univ Sao Paulo, Fac Med Ribeirao Preto, Programa Posgrad Farmacol, Ribeirao Preto, SP - Brazil
[4] Univ Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, Programa Posgrad Toxicol, Ribeirao Preto, SP - Brazil
[5] Alves, Juliano, V, Univ Sao Paulo, Fac Med Ribeirao Preto, Programa Posgrad Farmacol, Ribeirao Preto, SP - Brazil
Total Affiliations: 5
Document type: Journal article
Source: Canadian Journal of Physiology and Pharmacology; v. 99, n. 12, p. 1324-1332, DEC 2021.
Web of Science Citations: 0
Abstract

We tested the hypothesis that ethanol would aggravate the deleterious effects of sub-lethal cecal ligation and puncture (SL-CLP) sepsis in the cardiorenal system and that inhibition of inducible nitric oxide synthase (iNOS) would prevent such response. Male C57BL/6 mice were treated with ethanol for 12 weeks. One hour before SL-CLP surgery, mice were treated with N-6-(1-iminoethyl)-lysine (L-NIL, 5 mg/kg, i.p.), a selective inhibitor of iNOS. A second dose of L-NIL was administered 24 h after SL-CLP surgery. Mice were killed 48 h post surgery and the blood, the renal cortex, and the left ventricle (LV) were collected for biochemical analysis. L-NIL attenuated the increase in serum creatinine levels induced by ethanol, but not by SL-CLP. Ethanol, but not SL-CLP, increased creatine kinase (CK)-MB activity and L-NIL did not prevent this response. In the renal cortex, L-NIL prevented the redox imbalance induced by ethanol and SL-CLP. Inhibition of iNOS also decreased lipoperoxidation induced by ethanol and SL-CLP in the LV. L-NIL prevented the increase of pro-inflammatory cytokines and reactive oxygen species induced by ethanol and (or) SL-CLP in the cardiorenal system, suggesting that iNOS modulated some of the molecular mechanisms that underlie the deleterious effects of both conditions in the cardiorenal system. (AU)

FAPESP's process: 17/24123-5 - Impact of chronic ethanol consumption in the cardiac and vascular damages induced by experimental sepsis: evaluation of the role of iNOS
Grantee:Carlos Renato Tirapelli
Support Opportunities: Regular Research Grants
FAPESP's process: 18/06583-1 - Role of iNOS in the renal alterations induced by experimental sepsis in rats chronically treated with ethanol
Grantee:Arthur Henrique de Sousa
Support Opportunities: Scholarships in Brazil - Scientific Initiation
FAPESP's process: 18/23985-6 - Impact of chronic ethanol consumption on the cardiac lipoperoxidation and oxidative stress induced by experimental sepsis: role of iNOS
Grantee:Jose de Araujo Nascimento
Support Opportunities: Scholarships in Brazil - Scientific Initiation