动物造模,帕金森病模型 z-bio 2021-04-02 785

　　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. Principles 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 continuous 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 generated in the substantia nigra cells, breaking through the protective barrier of the substantia nigra cytochrome and causing cell death.

　　4. Changes after modeling The neurons in the normal control group are basically intact, and the manganese chloride in the model group damages more than 80% of the rat's dopaminergic neurons. 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, and 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.