Apoptotic mechanisms in rabbits with blast-induced acute lung injury

Abstract

To investigate the apoptotic mechanisms in rabbits with blast-induced acute lung injury (ALI). Methods: A total of 40 rabbits were randomly divided into a blank control group (A, n=10) and an experimental group (EXP, n=30). Explosion-induced chest-ALI models were prepared and sampled at different time points (4, 12, and 24h after modeling, T1-T3) to test the lung dry weight/wet weight ratio (W/D) and arterial oxygen pressure (PaO 2), apoptosis of lung tissue by the TUNEL assay, and Caspase-3, Bax, and Bcl-2 levels by immunohistochemical analysis. Furthermore, lung tissue was sampled to observe pathological morphology by microscopy. Results: Under a light microscope, Group EXP exhibited obvious edema in the pulmonary interstitial substance and alveoli, a large number of red blood cells, inflammatory cells, and serous exudation in the alveolar cavity, as well as thickening of the pulmonary interstitial fluid. Compared to Group A, the W/D ratio was significantly increased in Group EXP (P<0.01), while PaO 2 was significantly reduced (P<0.01). The apoptosis index was significantly increased (P<0.01), and caspase-3 and Bax/Bcl-2 levels were increased (P<0.01). Conclusion: Apoptosis plays an important role in the occurrence and development of acute lung injury in rabbits by participating in lung injury and promoting the progression of ALI.

Effect of Exosomes Derived From Bone Marrow Mesenchymal Stem Cells on Programmed Cell Death in Blast-Induced Lung Injury in Rats

“…The downstream caspase apoptosis executive protein subsequently initiates the cell death process. Recently, some scholars have pointed out that in a rabbit model of blast-induced lung injury, apoptosis accelerates ALI progression (47). In addition, studies have found that Tanshinone IIA has been shown to protect against lung blast damage, possibly by inhibiting oxidative stress and apoptosis.…”

Gas explosion-induced acute blast lung injury assessment and biomarker identification by a LC-MS-based serum metabolomics analysis

“…Numerous studies have demonstrated that the damage effects of gas explosion both existed in animal models and in humans. [16][17][18] Epidemiological studies have suggested that gas explosion was related to multiple respiratory disorders, such as pulmonary fibrosis and chronic obstructive pulmonary disease. 3 However, the pathological mechanism underlying gas explosion-induced ABLI is still not completely clarified.…”

“…A study have shown that apoptosis plays an important role in the occurrence and development of acute lung injury (ALI) in rabbits by participating in lung injury and promoting the progression of ALI. 17 The last marker analyzed to understand the metabolomics of gas explosion-induced ABLI was an Llysine, which belongs to the class of foundational amino acids. L-lysine plays important roles in the immune system in the liver, and acts as an antiinflammatory to the entire nervous system, especially the central nervous system.…”

“…A study have shown that apoptosis plays an important role in the occurrence and development of acute lung injury (ALI) in rabbits by participating in lung injury and promoting the progression of ALI. 17…”

Genomics and the Acute Respiratory Distress Syndrome: Current and Future Directions

“…Among many others, cell-free mitochondrial DNA (mtDNA) and mitochondrial peptides are endogenous damage-associated molecular patterns (DAMPs) [24,25], which are also known to play a critical role in modulating the response to pulmonary injury [26,27]. Linked to this, lung injury can be triggered by failures in cell division through diverse proteins related to apoptosis, such as Bax, Bcl-2 and cleaved-caspase-3, which are also known as biomarkers of lung injury [28], as their levels change markedly during the early stages of the disease process [29]. In fact, some studies in experimental animal models have focused on the therapeutic use of microRNA targets to reduce apoptosis and, concomitantly, the levels of inflammatory factors such as interleukin (IL)-1β (IL-1β) and tumour necrosis factor alpha (TNF-α) during experimental ARDS [30].…”