Abstract
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.
Highlights
The present study aimed to evaluate the effects of dexamethasone on the redox status, parasitemia evolution, and survival rate of Plasmodium berghei-infected mice
Parasitemia of infected animals progressively evolved in all groups, but the rate of progression was lower in dexamethasone-treated animals, which presented lower parasitemia values than the other two groups at the end of the period of 20 days (p = 2.8 × 10−5 vs. L-arginine and p = 0.0227 vs. control; Fig. 1)
After the 10th day of infection, the DEXAMETHASONE group presented an increase in Trolox Equivalent Antioxidant Capacity (TEAC) values, displaying statistically higher values than the other groups (p = 0.0357 vs. L-ARGININE and p = 0.0005 vs. POSITIVE CONTROL: Fig. 3B)
Summary
The present study aimed to evaluate the effects of dexamethasone on the redox status, parasitemia evolution, and survival rate of Plasmodium berghei-infected mice. 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. According to the World Health Organization (WHO), malaria is a significant public health problem in 97 countries and causes approximately 219 million new cases each year, resulting in 435,000 deaths in 2 0171. In this regard, several authors recently discussed the involvement of free radicals in the physiopathogenesis of malaria. It is still unknown whether the major problem arises from insufficient concentrations of N O11 acting directly in the elimination of the parasite, and for this reason, by selecting more resistant strains of the parasite, or from the high concentrations of NO produced as a result of infection by the protozoan parasite and responsible for cerebral e dema[12,13]
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