| Autor: |
de Souza Gomes R; Pharmaceutical Science Post-Graduation Program, Faculty of Pharmacy, Federal University of Pará, Pará 66075110, Brazil. rafaelli_gomes@hotmail.com., Navegantes-Lima KC; Pharmaceutical Science Post-Graduation Program, Faculty of Pharmacy, Federal University of Pará, Pará 66075110, Brazil. kcnavegantes@gmail.com.; Neuroscience and Cellular Biology Post Graduation Program, Institute of Biological Sciences, Federal University of Pará, Pará 66075110, Brazil. kcnavegantes@gmail.com., Monteiro VVS; Laboratory of Inflammation and Pain, Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, São Paulo 14049900, Brazil. valterv@live.com., de Brito Oliveira AL; Pharmaceutical Science Post-Graduation Program, Faculty of Pharmacy, Federal University of Pará, Pará 66075110, Brazil. any_015_@hotmail.com.; Neuroscience and Cellular Biology Post Graduation Program, Institute of Biological Sciences, Federal University of Pará, Pará 66075110, Brazil. any_015_@hotmail.com., Rodrigues DVS; School of Pharmacy, Health Science Institute, Federal University of Pará, Pará 66075110, Brazil. davilavrodrigues@gmail.com., Reis JF; School of Pharmacy, Health Science Institute, Federal University of Pará, Pará 66075110, Brazil. jordanoreis@outlook.com., Gomes ARQ; Pharmaceutical Science Post-Graduation Program, Faculty of Pharmacy, Federal University of Pará, Pará 66075110, Brazil. rafaelquadros13@hotmail.com.; Pharmaceutical Innovation Post-Graduation Program, Institute of Health Sciences, Federal University of Pará, Pará 66075110, Brazil. rafaelquadros13@hotmail.com., Prophiro JS; Department of Biological Sciences and Health, University of Southern Santa Catarina, Santa Catarina 88704900, Brazil. josiane.prophiro@hotmail.com., da Silva OS; Department of Microbiology, Immunology and Parasitology, Basic Health Sciences Institute, Federal University of Rio Grande do Sul, Rio Grande do Sul 90040060, Brazil. onilda.santos@gmail.com., Romão PRT; Laboratory of Cellular and Molecular Immunology, Department of Basic Sciences, Federal University of Health Sciences of Porto Alegre, 90050170, Brazil. pedror@ufcspa.edu.br., Estrada JEC; Neuroscience and Cellular Biology Post Graduation Program, Institute of Biological Sciences, Federal University of Pará, Pará 66075110, Brazil. jorgechang01@gmail.com., Monteiro MC; Pharmaceutical Science Post-Graduation Program, Faculty of Pharmacy, Federal University of Pará, Pará 66075110, Brazil. martachagas2@yahoo.com.br.; Neuroscience and Cellular Biology Post Graduation Program, Institute of Biological Sciences, Federal University of Pará, Pará 66075110, Brazil. martachagas2@yahoo.com.br. |
| Abstrakt: |
Sepsis is a systemic disease with life-threatening potential and is characterized by a dysregulated immune response from the host to an infection. The organic dysfunction in sepsis is associated with the production of inflammatory cascades and oxidative stress. Previous studies showed that Aedes aegypti saliva has anti-inflammatory, immunomodulatory, and antioxidant properties. Considering inflammation and the role of oxidative stress in sepsis, we investigated the effect of pretreatment with salivary gland extract (SGE) from Ae. aegypti in the induction of inflammatory and oxidative processes in a murine cecum ligation and puncture (CLP) model. Here, we evaluated animal survival for 16 days, as well as bacterial load, leukocyte migration, and oxidative parameters. We found that the SGE pretreatment improved the survival of septic mice, reduced bacterial load and neutrophil influx, and increased nitric oxide (NO) production in the peritoneal cavity. With regard to oxidative status, SGE increased antioxidant defenses as measured by Trolox equivalent antioxidant capacity (TEAC) and glutathione (GSH), while reducing levels of the oxidative stress marker malondialdehyde (MDA). Altogether, these data suggest that SGE plays a protective role in septic animals, contributing to oxidative and inflammatory balance during sepsis. Therefore, Ae. aegypti SGE is a potential source for new therapeutic molecule(s) in polymicrobial sepsis, and this effect seems to be mediated by the control of inflammation and oxidative damage. |
