动物模型,帕金森 z-bo 2022-03-25 472

　　1. Modeling materials Animal: SD rat, male, body weight (200±10) g; drug: manganese chloride reagent.

　　2. Modeling method SD rats were intraperitoneally injected with 50mg/kg MnCl2 solution, and the normal control group was intraperitoneally injected with an equal volume of normal saline, once a day for 7 days.

　　3. Principle of Modeling Manganese can cause PD, and its main mechanism is: the melanin neurons and dopaminergic neurons distributed in the dense zone of the substantia nigra have the effect of enriching and accumulating metal elements such as manganese. The continuous release of accumulated manganese can cause sustained extrapyramidal neurotoxicity. Therefore, manganese acts as a triggering factor to act on the dopamine synapse, enhancing its conversion. Through the interaction of manganese and dopamine, a large number of free radicals are produced in the substantia nigra cells, breaking through the protective barrier of substantia nigra cytochromes and causing cell death.

　　4. Changes after modeling The neurons in the normal control group were basically intact, and the manganese chloride in the model group damaged more than 80% of the dopaminergic neurons in the rat. Normal control group: the neurons are intact, and the substantia nigra compact part is arranged in a crescent shape; the model group: the surviving neurons are severely missing and the arrangement is disordered.

　　The blood levels of interleukin-2 (IL-2) and tumor necrosis factor-α (TNF-α) showed that the model group was significantly higher than the normal control group. The normal control group Group (1.85±0.23) ng/ml, (0.46±0.08) ng/ml, model group (3.25±0.60) ng/ml, (1.08±0.09) ng/ml.