Douglas Soares de Oliveira
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Douglas Soares de Oliveira has a total of 15 co-authors. Here are the top co-authors by number of shared publications:
- Airton Lucas Sousa dos Santos
Infectious Disease Laboratory, Campus Ministro Reis Velloso, Federal University of Parnaíba Delta, Parnaíba 64202-020, PI, Brazil
1 shared publication - Edeildo Ferreira da Silva-Júnior
Biological and Molecular Chemistry Research Group, Institute of Chemistry and Biotechnology, Federal University of Alagoas, Maceió 57072-900, AL, Brazil
1 shared publication - Francisco Jaime Bezerra Mendonça-Junior
Laboratory of Synthesis and Drug Delivery, Department of Biological Sciences, State University of Paraíba, João Pessoa 58071-160, Brazil
1 shared publication - Ingrid Gracielle Martins da Silva
Microscopy and Microanalysis Laboratory, Department of Cell Biology, Institute of Biological Sciences, University of Brasília, Brasília 70910-900, DF, Brazil
1 shared publication - Julyanne Maria Saraiva de Sousa
Infectious Disease Laboratory, Campus Ministro Reis Velloso, Federal University of Parnaíba Delta, Parnaíba 64202-020, PI, Brazil
1 shared publication - Karine Brenda Barros-Cordeiro
Universidade de Brasília; Departamento de Zoologia; Brasília; DF; 70910-900; Brazil
1 shared publication
Latest Publications
- Open Access
2-Aminothiophene Derivative SB-83 Inhibits Trypanothione Reductase and Modulates Cytokine Production in Trypanosoma cruzi-Infected Cells
Chagas disease remains a significant neglected tropical disease that predominantly affects vulnerable populations in rural, low-income areas of Latin America. The management of this condition is severely hindered by the limitations of current therapies, which are characterized by substantial toxicity, diminished efficacy during the chronic phase, and the emergence of parasitic resistance. Given the promising activity of SB-83 (a 2-aminothiophenic derivative) against Leishmania spp., the present study sought to evaluate its trypanocidal activity against Trypanosoma cruzi. The results showed that SB-83 exhibited potent inhibitory effects on the epimastigote forms of T. cruzi (IC50 = 6.23 ± 0.84 μM), trypomastigotes (EC50 = 7.31 ± 0.52 μM) and intracellular amastigotes (EC50 = 5.12 ± 0.49 μM). Furthermore, the cellular proliferation assay results indicated CC50 values of 77.80 ± 2.05 µM for LLC-MK2 CCL-7 and 24.21 ± 1.2 µM for Vero CCL-87, with a selectivity index above 10 for LLC-MK2 cells. In addition, the compound increased TNF-α, IL-12, nitric oxide, and ROS while decreasing IL-10. Moreover, in silico and in vitro assays confirmed its binding to trypanothione reductase, disrupting redox balance. Flow cytometry further revealed apoptosis induction in trypomastigotes, whereas electron microscopy showed cellular disruption and organelle disorganization. Therefore, SB-83 demonstrated potent activity against the TcI-resistant strain linked to Chagas cardiomyopathy at non-toxic concentrations for host cells, supporting its potential as a therapeutic candidate.
Open Access2-Aminothiophene Derivative SB-83 Inhibits Trypanothione Reductase and Modulates Cytokine Production in Trypanosoma cruzi-Infected Cells
Chagas disease remains a significant neglected tropical disease that predominantly affects vulnerable populations in rural, low-income areas of Latin America. The management of this condition is severely hindered by the limitations of current therapies, which are characterized by substantial toxicity, diminished efficacy during the chronic phase, and the emergence of parasitic resistance. Given the promising activity of SB-83 (a 2-aminothiophenic derivative) against Leishmania spp., the present study sought to evaluate its trypanocidal activity against Trypanosoma cruzi. The results showed that SB-83 exhibited potent inhibitory effects on the epimastigote forms of T. cruzi (IC50 = 6.23 ± 0.84 μM), trypomastigotes (EC50 = 7.31 ± 0.52 μM) and intracellular amastigotes (EC50 = 5.12 ± 0.49 μM). Furthermore, the cellular proliferation assay results indicated CC50 values of 77.80 ± 2.05 µM for LLC-MK2 CCL-7 and 24.21 ± 1.2 µM for Vero CCL-87, with a selectivity index above 10 for LLC-MK2 cells. In addition, the compound increased TNF-α, IL-12, nitric oxide, and ROS while decreasing IL-10. Moreover, in silico and in vitro assays confirmed its binding to trypanothione reductase, disrupting redox balance. Flow cytometry further revealed apoptosis induction in trypomastigotes, whereas electron microscopy showed cellular disruption and organelle disorganization. Therefore, SB-83 demonstrated potent activity against the TcI-resistant strain linked to Chagas cardiomyopathy at non-toxic concentrations for host cells, supporting its potential as a therapeutic candidate.