ArticleParasites & vectors2025
Upregulation of Nrf2 attenuates Angiostrongylus cantonensis-induced parasitic meningitis in mice.
Article in Parasites & vectors, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
backgroundAngiostrongylus cantonensis is a food-borne parasite that can infect mammals, including humans, causing angiostrongyliasis. The nuclear factor E2-related factor 2 (Nrf2) is a transcription factor that plays a crucial role in the host's antioxidant defense and inflammation mechanisms. Herein, this study investigates the anti-inflammatory effects of Nrf2 in A. cantonensis-induced parasitic meningitis in mice.
methodsWe used animal infection and treatment, larvae collection, western blotting, enzyme-linked immunosorbent assay (ELISA), hematoxylin and eosin (H&E) stain, blood-brain barrier (BBB) permeability assays, and an NAD(P)H quinone dehydrogenase 1 (NQO1) enzyme activity, reactive oxygen species (ROS), and superoxide dismutase (SOD) assay kit in this study.
resultsOur findings revealed that larvae recovery, BBB permeability, and inflammatory mediators (interleukin (IL)-1β, IL-6, IL-17A, and tumor necrosis factor (TNF)-α) were increased in A. cantonensis-infected mice. However, p-Nrf2 levels were slightly increased in infected groups. To better understand the modulatory role of Nrf2 in the parasitic meningitis, we also treated A. cantonensis-infected mice with oltipraz (an Nrf2 activator) and trigonelline (an Nrf2 inhibitor). The larvae recovery, BBB permeability, and levels of inflammatory mediators were significantly decreased in the albendazole alone, oltipraz, and albendazole-oltipraz co-treatment groups, particularly in albendazole-oltipraz co-treatment groups. In contrast, trigonelline treatment resulted in increased levels of larvae recovery, BBB permeability, and inflammatory mediators. Moreover, since Nrf2 is involved in the regulation of antioxidant enzymes, we also examined the expression of ROS, NQO1, and SOD. ROS levels were significantly increased in infected groups but decreased in the albendazole alone, oltipraz alone, and albendazole-oltipraz co-treatment groups. NQO1 and SOD levels were significantly decreased in infected groups, but these levels were notably restored during treatment with albendazole alone, oltipraz alone, and albendazole-oltipraz co-treatment.
conclusionsOur findings revealed the albendazole-Nrf2 activator co-treatment effectively suppressed excessive inflammation compared with the anthelmintics drug (albendazole) treatment alone, and Nrf2 activation might produce a synergistic effect in the inflammatory response of the brain in mice with angiostrongyliasis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.