The decrease on Na(+), K(+)-ATPase activity in the cortex, but not in hippocampus, is reverted by antioxidants in an animal model of sepsis.
In the present study, we investigated whether sepsis induced by cecal ligation and puncture (CLP) modifies Na(+), K(+)-ATPase activity, mRNA expression, and cerebral edema in hippocampus and cerebral cortex of rats and if antioxidant (ATX) treatment prevented the alterations induced by sepsis. Rats were subjected to CLP and were divided into three groups: sham; CLP-rats were subjected to CLP without any further treatment; and ATX-CLP plus administration of N-acetylcysteine plus deferoxamine. Several times (6, 12, and 24) after CLP or sham operation, the rats were killed and hippocampus and cerebral cortex were isolated. Na(+), K(+)-ATPase activity was inhibited in the hippocampus 24 h after sepsis, and ATX treatment was not able to prevent this inhibition. The Na(+), K(+)-ATPase activity also was inhibited in cerebral cortex 6, 12, and 24 h after sepsis. No differences on Na(+), K(+)-ATPase catalytic subunit mRNA levels were found in the hippocampus and cerebral cortex after sepsis. ATX treatment prevents Na(+), K(+)-ATPase inhibition only in the cerebral cortex. Na(+), K(+)-ATPase inhibition was not associated to increase brain water content. In conclusion, the present study demonstrated that sepsis induced by CLP inhibits Na(+), K(+)-ATPase activity in a mechanism dependent on oxidative stress, but this is not associated to increase brain water content.
Laboratório de Fisiopatologia Experimental, Programa de Pós-graduação em Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil.
Isabela Casagrande
IC
Jeremias
Giselli
G
Scaini
Larissa
L
Constantino
Francieli
F
Vuolo
Andreia Kurek
AK
Ferreira
Emilene Barros Silva
EB
Scherer
Janaina
J
Kolling
Arethuza
A
da Silva Dornelles
Angela Terezinha
AT
de Souza Wyse
Maurício Reis
MR
Bogo
Felipe
F
Dal-Pizzol
Emilio Luiz
EL
Streck
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D020134:Catalytic Domain; D002540:Cerebral Cortex / Q000187:drug effects / Q000201:enzymology* / Q000473:pathology; D004195:Disease Models, Animal; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D006624:Hippocampus / Q000187:drug effects / Q000201:enzymology* / Q000473:pathology; D008297:Male; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D018805:Sepsis / Q000201:enzymology* / Q000235:genetics / Q000473:pathology*; D000254:Sodium-Potassium-Exchanging ATPase / Q000235:genetics / Q000378:metabolism*; D014867:Water / Q000378:metabolism
D000975:Antioxidants; D012333:RNA, Messenger; D014867:Water; D000254:Sodium-Potassium-Exchanging ATPase