1. Animal modeling materials: Newborn 1-day old Wistar rat offspring, male and female, weighing 5-10g.
2. Modeling method: First, inject carbon dioxide into the hypoxic chamber, adjust the flow rate, and use the RSS-5100 portable digital oxygen meter to measure the concentration of carbon dioxide in the chamber to reach 100% [maintained at (99.9 ± 0.2)%]. After that, place the 1-day old newborn mice in the chamber for 5 minutes and remove them. Quickly inject oxygen into the oxygen chamber, and use an oxygen meter to maintain the concentration in the chamber to 100% [maintained at (99.0 ± 0.8)%]. Then, place the hypoxic newborn mice in the chamber for 5 minutes and remove them.
3. Modeling principle: Hypoxia can reduce mucosal blood flow and induce early changes in capillary endothelial cells, ultimately leading to intestinal necrosis.
4. Changes after modeling: TNF in the tissue homogenate supernatant of the model group- α The content of (39.957 ± 8.283) pg/mg total protein was higher than that of the control group (33.523 ± 6.752) pg/mg total protein, and the NO content in the model group was (0.82 ± 0.04) μ Mol/mg tissue was higher than the control group (0.41 ± 0.02) μ Mol/mg tissue.
The model group showed positive expression of inducible nitric oxide synthase (iNOS) in inflammatory cells and smooth muscle cells of intestinal tissue, as well as in some intestinal epithelial cells. The number of positive particles and staining intensity were significantly higher than those in the control group. Image analysis showed that the positive staining area ratio × The average luminosity is 3.01 ± 0.71; The score range of pathological and histological changes in the model group is 1-4 points, with a median score of 3 points, ranging from superficial epithelial injury with shortened villi to complete mucosal necrosis.