Expressions of apoptotic protein and gene following sulfur mustard-induced acute pulmonary injuries in rats
نویسندگان
1 Department of Respiration, the 80th Group Army Hospital of People’s Liberation Army, Weifang, 261021, China
2 State Key Laboratory of Antitoxic Drugs and Toxicology, Institute of Toxicology and Pharmacology, Academy of Military Medical Sciences, Beijing, 100850, China
3 Department of Respiration, the 80th Group Army Hospital of People’s Liberation Army, Weifang, 261021, China
4 State Key Laboratory of Antitoxic Drugs and Toxicology, Institute of Toxicology and Pharmacology, Academy of Military Medical Sciences, Beijing, 100850, China
5 Department of Respiration, the 80th Group Army Hospital of People’s Liberation Army, Weifang, 261021, China
6 Department of Pulmonary and Critical Care Medicine, Weifang No. 2 People’s Hospital, Weifang Respiratory Disease Hospital, Weifang, 261041, China
7 Department of Dermatology, The Third Medical Center of Chinese PLA General Hospital, Beijing, 100039, China
doi
10.22038/ijbms.2025.86449.18678چکیده
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 (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.
