ArticleOpen medicine (Warsaw, Poland)2026
Exogenous H
Article in Open medicine (Warsaw, Poland), 2026. 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
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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.
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.
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0 citing papers in PubMed.
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Traumatic stress triggers systemic inflammation and organ injury via HMGB1 and endoplasmic reticulum stress (ERS), but whether H Methods: Male SD rats underwent bilateral hindlimb crush. Sixty rats were assigned to sham, crush, NaHS pretreatment (14, 28, 56 μmol/kg), delayed NaHS (120 μmol/kg), and NaHS-only groups (n=6). Serum ALT/AST, histopathology, HMGB1 (ELISA/IHC), and ERS markers (GRP78, caspase-12, CHOP, IRE1α) were assessed. Results: Crush increased ALT/AST, liver/lung injury, plasma HMGB1, cytoplasmic HMGB1 translocation, and ERS activation. NaHS at 28 μmol/kg offered strongest protection, reducing all parameters. The 14 μmol/kg dose had limited effect; 56 μmol/kg showed reduced efficacy and mild toxicity. Delayed 120 μmol/kg also attenuated injury and HMGB1-ERS activation, though less effectively than 28 μmol/kg pretreatment. Conclusions: Exogenous H
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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.