ArticleIranian journal of basic medical sciences2025
Expressions of apoptotic protein and gene following sulfur mustard-induced acute pulmonary injuries in rats.
Article in Iranian journal of basic medical sciences, 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Pathomechanisms of sulfur mustard (SM) are not fully understood, and no specific medical countermeasures exist to prevent SM-induced pulmonary injury. This study aimed to evaluate the apoptosis following SM-induced acute pulmonary injury. Materials and Methods: Acute pulmonary injury models were established using SM at an equivalent toxicity dose (1 LD50), administered via intraperitoneal injection or intratracheal instillation. Protein expression levels and mRNA expressions of apoptosis-related markers, including cellular inhibitor of apoptosis proteins-1 and -2 (cIAP-1, cIAP-2), Fas, Bcl-2-associated death promoter (Bad), second mitochondria-derived activator of caspases (Smac), and survivin (BIRC5), were analyzed using immunohistochemistry and polymerase chain reaction. Results: The intraperitoneal SM group exhibited significantly higher levels of apoptotic cells in the alveolar septa and increased protein and mRNA expression of cIAP-1, cIAP-2, Fas, Bad, Smac, and BIRC5 compared to the intratracheal SM group. These changes displayed a time-dependent increase in both protein and gene expression levels. Conclusion: SM-induced pulmonary injury involves both extrinsic (Fas, cIAP-1, cIAP-2) and intrinsic (Bad, Smac) pathways as well as caspase-dependent pathways (BIRC5). These findings provide valuable insights into the underlying mechanisms of SM toxicity and may facilitate the development of targeted therapeutic strategies.
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.