ArticleParasitology research2013
The specific, reversible JNK inhibitor SP600125 improves survivability and attenuates neuronal cell death in experimental cerebral malaria (ECM).
Article in Parasitology research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Effects of anti-tau immunotherapy on reactive microgliosis, cerebral endotheliopathy, and cognitive function in an experimental model of cerebral malaria.Journal of neurochemistry · 2023Article
- The roles of COX-2 in protozoan infection.Frontiers in immunology · 2023Review
- NOD1 and NOD2 Activation by Diverse Stimuli: a Possible Role for Sensing Pathogen-Induced Endoplasmic Reticulum Stress.Infection and immunity · 2020Review
- JNK, p38, ERK, and SGK1 Inhibitors in Cancer.Cancers · 2017Article
- The p38 MAPK inhibitor, SB203580, inhibits cell invasion by Neospora caninum.Parasitology research · 2017Article
- Host-pathogen interactions in malaria: cross-kingdom signaling and mitochondrial regulation.Current opinion in immunology · 2015Review
- Myeloid expression of the AP-1 transcription factor JUNB modulates outcomes of type 1 and type 2 parasitic infections.Parasite immunology · 2015Article
- Endothelin-1 and its role in the pathogenesis of infectious diseases.Life sciences · 2014Review
- Reduction of experimental cerebral malaria and its related proinflammatory responses by the novel liposome-based β-methasone nanodrug.BioMed research international · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
Cerebral malaria (CM) is the most severe complication of Plasmodium falciparum in humans and major cause of death. SP600125 is a specific, small molecule inhibitor of JNK that prevents the phosphorylation of c-Jun and blocks the expression of proinflammatory cytokines and attenuates neuronal apoptosis in several neurodegenerative disorders. We evaluated the effect of SP600125 treatment on the survival of Plasmodium berghei ANKA (PbA)-infected C57BL/6J mice. Administration of SP600125 improved survival in PbA-infected C57BL6J mice but has no effect on parasitemia. Further, SP600125 administration resulted in attenuation of neuronal cell death along with inhibition of proinflammatory mediators TNF-α and COX-2 and proapoptotic mediators p-c-Jun and active caspase 3 in PbA-infected mice. The promising findings of this study make SP600125 a potential agent for supportive therapy to alleviate inflammation and neuronal cell death associated with CM.
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