ArticleMolecular medicine reports2017
Hydrogen sulfide protects against the development of experimental cerebral malaria in a C57BL/6 mouse model.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Impact of Reactive Sulfur Species onAntioxidants (Basel, Switzerland) · 2024Article
- Therapeutic Potential of Carbon Monoxide (CO) and Hydrogen Sulfide (HInternational journal of molecular sciences · 2020Review
- The H₂S Donor GYY4137 Stimulates Reactive Oxygen Species Generation in BV2 Cells While Suppressing the Secretion of TNF and Nitric Oxide.Molecules (Basel, Switzerland) · 2018Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hydrogen sulfide (H2S) has anti‑inflammatory and neuroprotective properties, particularly during pathological processes. Experimental cerebral malaria (ECM), which is caused by vascular leakage into the brain, is characterized by inflammation, neurological deficits and cerebral hemorrhage. The present study investigated the correlation between ECM genesis and the levels of H2S. The results indicated that the levels of H2S derived from the brain decreased over time following ECM infection, and that the low H2S bioavailability was partially caused by decreased expression of the H2S generating enzyme, cystathionine‑β‑synthase. Administration of NaHS (an exogenous donor of H2S) provided protection against ECM. NaHS inhibited the destruction of the blood brain barrier and the secretion of proinflammatory biomarkers, including interluekin‑18, matrix metalloproteinase‑9 and serum cluster of differentiation 40 into the brain during ECM. In conclusion, these results suggested that low levels of H2S in brain contributed to the progression of ECM, and that H2S donor administration may represent a potential protective therapy against ECM.
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