[Animal Modeling]-Damaged hypothalamic arcuate nucleus atherosclerosis model

  (1) Replication method Neonatal Wistar rats were injected with 10% monosodium glutamate (MSG) at a dose of 4 g/kg body weight on the 1, 3, 5, 7 and 9 days after birth. 5 times. Thirty days after MSG injection, the aorta was harvested for electron microscopy. It can be seen that there are microvilli-like protrusions in the endothelial cell lumen of the aortic wall, the endothelial cell nucleus is somewhat distorted and irregular, and the endothelium is not thickened; 60 days after the injection of MSG. The animal's blood vessel wall degenerates and falls off, resulting in obvious thickening of the subepithelial layer. Many vacuoles of varying sizes and proliferative collagen fibers, macrophages and smooth muscle cells migrate to the endothelium.

  (2) As a model, the arcuate nucleus of the hypothalamus is destroyed by injection of MSG, ignoring the pathological process of the blood vessel itself. The As model is copied from the "central mechanism". Long-term stimulation of the rabbit hypothalamus can cause hyperlipidemia. This is a simple method compared with similar models, such as destroying the formation of the hypothalamus and aggravating coronary atherosclerosis. The results have the advantages of accurate quantification and reliability.

  (3) Comparison of animal histopathological characteristics after the establishment of this model: aortic wall endothelial cell degeneration, nucleus, subepithelial thickening, vacuoles, smooth muscle cells. These changes are consistent with the characteristic lesions of early clinical onset As; A substance closely related to the formation of As will also change, total cholesterol (TC). ), oxidized low-density lipoprotein (OX? LDL) and lipid peroxide (LPO) increase, while nitric oxide (NO) decreases. These changes are very similar to the changes in As caused by drugs. This model can be used as a model to explore the formation mechanism of central hypothalamic arcuate nucleus and As.