1. Animal modeling materials: Healthy SD rats, male or female, weighing (210 ± 23) g; Drug: Pingyangmycin, physiological saline; Instrument: Syringe.
2. Mold making method: Inject BLMA5 (5mg/kg) into the trachea of the mold at once. The blank control group received a one-time infusion of 0.5ml of physiological saline solution into the trachea.
3. Modeling principle: Injecting Pingyangmycin into the trachea can induce lung injury in animals.
4. Histopathological results of changes after modeling: The model group rats showed varying degrees of alveolitis at different stages, with the most severe on day 7. Under the light microscope, a large number of inflammatory cells infiltrated the alveolar cavity and interstitium, and some alveolar cavities were destroyed or disappeared. The alveolar walls thickened, and by the 28th day, pulmonary interstitial fibrosis occurred, mostly moderate to severe. Under the light microscope, significant thickening of the alveolar walls was observed, and the alveolar structure was disordered. The alveolar cavity was occupied by collagen fibers, fibroblasts, and lymphocytes. Under Masson staining, a significant increase in collagen fibers can be observed in the interstitial tissue of the lungs. The lung histology of the blank control group was normal.
On the 7th day, the lung tissue LPO [malondialdehyde (MDA) content, nmol/g] in the model group was significantly increased compared to the blank control group at 10.24 ± 0.67. On the 14th day, it tended to decrease at 14.53 ± 1.2, and on the 28th day, it decreased more significantly at 12.63 ± 1.35, but still higher than the blank control group.
On the 7th day, the hydroxyproline (HP) content (nmol/g) in the model group was 1.68 ± 0.45, which was significantly higher than that in the blank control group (0.77 ± 0.23), and continued to increase at 3.06 ± 0.37 on the 28th day.