Expressions of apoptotic protein and gene following sulfur mustard-induced acute pulmonary injuries in rats

Objective(s): 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 (۱ LD۵۰), administered via intraperitoneal injection or intratracheal instillation. Protein expression levels and mRNA expressions of apoptosis-related markers, including cellular inhibitor of apoptosis proteins-۱ and -۲ (cIAP-۱, cIAP-۲), Fas, Bcl-۲-associated death promoter (Bad), second mitochondria-derived activator of caspases (Smac), and survivin (BIRC۵), 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-۱, cIAP-۲, Fas, Bad, Smac, and BIRC۵ 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-۱, cIAP-۲) and intrinsic (Bad, Smac) pathways as well as caspase-dependent pathways (BIRC۵). These findings provide valuable insights into the underlying mechanisms of SM toxicity and may facilitate the development of targeted therapeutic strategies.

کلیدواژه ها:

Animals ، Apoptosis ، immunohistochemistry ، Lung injury ، Mustard Gas ، Polymerase chain reaction