Dimethyl fumarate reduces TNF and Plasmodium falciparum induced brain endothelium activation in vitro.

ABSTRACT:

Background

Cerebral malaria (CM) is associated with morbidity and mortality despite the use of potent anti-malarial agents. Brain endothelial cell activation and dysfunction from oxidative and inflammatory host responses and products released by Plasmodium falciparum-infected erythrocytes (IE), are likely the major contributors to the encephalopathy, seizures, and brain swelling that are associated with CM. The development of adjunctive therapy to reduce the pathological consequences of host response pathways could improve outcomes. A potentially protective role of the nuclear factor E2-related factor 2 (NRF2) pathway, which serves as a therapeutic target in brain microvascular diseases and central nervous system (CNS) inflammatory diseases such as multiple sclerosis was tested to

SUBMITTER: Mita-Mendoza NK 

PROVIDER: S-EPMC7579885 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature