[Animal modeling - efficacy evaluation] - Atherosclerosis model of hypothalamic arcuate nucleus lesion

  (1) Method of replication: Newborn Wistar rats were subcutaneously injected with 10% monosodium glutamate at a dose of 4g/kg body weight on the 1st, 3rd, 5th, 7th, and 9th day after birth, for a total of 5 injections. After injecting MSG for 30 days, the aorta was taken for electron microscopy observation. Microfurry like protrusions can be seen on the luminal surface of endothelial cells in the aortic wall, and the nuclei of endothelial cells are slightly twisted and irregular. No thickening is observed in the subendothelial layer; 60 days after injection of MSG, the endothelial cells in the animal blood vessel wall degenerated and shed, and the subendothelial layer thickened significantly. Many varying sizes of vacuoles and proliferating collagen fibers appeared, and macrophages and smooth muscle cells migrated into the subendothelial layer.

  (2) Model characteristics This model is different from the food and drug induced As model. It destroys the arcuate nucleus of the hypothalamus by injecting monosodium glutamate, bypassing the process of vascular disease itself, and replicates the As model from the "central mechanism". Compared with similar models, such as long-term stimulation of the rabbit hypothalamus can cause hyperlipemia and As formation, destruction of the hypothalamus can aggravate coronary atherosclerosis, it has the advantages of simple method, accurate quantification, and reliable results.

  (3) The histopathological characteristics of animals after modeling in comparative medicine include degeneration of endothelial cells in the aortic wall, swelling of cell nuclei, thickening and formation of vacuoles in the subendothelial layer, and visible migration of smooth muscle cells to the subendothelial layer. These changes are consistent with the characteristic lesions of early onset of As in clinical practice; The substances closely related to the formation of As in the blood also undergo changes, with an increase in total cholesterol (TC), oxidized low-density lipoprotein (OX-LDL), and lipid peroxides (LPO), while nitric oxide (NO) decreases. These changes are very similar to those induced by medication for As. This model can be used as a model to explore the mechanism of formation between the central hypothalamic arcuate nucleus and As.