Dexamethasone increased the survival rate in Plasmodium berghei-infected mice

被引:7
作者
Moreira, Danilo Reymao [1 ]
Musa Goncalves Uberti, Ana Carolina [1 ]
Quadros Gomes, Antonio Rafael [1 ]
Souza Ferreira, Michelli Erica [2 ]
Barbosa, Aline da Silva [1 ]
Pompeu Varela, Everton Luiz [1 ]
Dolabela, Maria Fani [3 ]
Percario, Sandro [1 ]
机构
[1] Fed Univ Para, Oxidat Stress Res Lab, Inst Biol Sci, Av Augusto Correa 01, BR-66075110 Belem, Para, Brazil
[2] Univ Fed Maranhao, Lab Pathophysiol & Therapeut Res, Ctr Ciencias Sociais Saude & Tecnol CCSST, Campus Avancado Bom Jesus,Predio Med,Av Univ S-N, BR-65915240 Imperatriz, MA, Brazil
[3] Fed Univ Para, Inst Hlth Sci, Av Augusto Correa 01, BR-66075110 Belem, Para, Brazil
关键词
NITRIC-OXIDE SYNTHASE; MURINE CEREBRAL MALARIA; GLUCOCORTICOIDS INHIBIT; OXIDATIVE STRESS; DOUBLE-BLIND; LUNG INJURY; L-ARGININE; EXPRESSION; FALCIPARUM; MODEL;
D O I
10.1038/s41598-021-82032-7
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The present study aimed to evaluate the effects of dexamethasone on the redox status, parasitemia evolution, and survival rate of Plasmodium berghei-infected mice. Two-hundred and twenty-five mice were infected with Plasmodium berghei and subjected to stimulation or inhibition of NO synthesis. The stimulation of NO synthesis was performed through the administration of L-arginine, while its inhibition was made by the administration of dexamethasone. Inducible NO synthase (iNOS) inhibition by dexamethasone promoted an increase in the survival rate of P. berghei-infected mice, and the data suggested the participation of oxidative stress in the brain as a result of plasmodial infection, as well as the inhibition of brain NO synthesis, which promoted the survival rate of almost 90% of the animals until the 15th day of infection, with possible direct interference of ischemia and reperfusion syndrome, as seen by increased levels of uric acid. Inhibition of brain iNOS by dexamethasone caused a decrease in parasitemia and increased the survival rate of infected animals, suggesting that NO synthesis may stimulate a series of compensatory redox effects that, if overstimulated, may be responsible for the onset of severe forms of malaria.
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页数:12
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