Construction method of transgenic zebrafish (mbp:egfp) spinal cord removal disease model

Abstract

The invention discloses a construction method of a transgenic fish (mbp:egfp) demyelinating disease model established by using a drug scopoletin, and the method comprises the following steps: placing the transgenic fish (mbp:egfp) in a 18.5 [mu] g / ml scopoletin solution, and completing the construction of a zebra fish model after 3-6 days. By combining various factors such as genes, environment, aging and the like, the zebrafish demyelination disease model can be quickly constructed, and a basis is provided for a mechanism and a treatment method of the demyelination disease.

Description

Technical field [0001] The present invention is in the field of biomedicine, in particular to a zebrafish gene transfer: spinal cord removal method of constructing a disease model (mbp egfp). Background technique [0002] Before the onset of demyelinating disease is an acute or subacute disease damages the nerve center, the peak incidence is two to three weeks, if the delay in treatment of damaged nerve degeneration secondary to ischemia and multiple sclerosis occurs, the incidence of serious violations of the spinal cord can horn cells and brainstem nucleus and the motor cortex pyramidal cells endanger the lives, mostly due to genetic abnormalities or immune virus infection. Early in the treatment of multiple hormonal and nutritional therapy, but the effect is difficult to control the solid, because the disease leads to demyelination induced nerve damage secondary to axonal damage so serious that the recurrence of neurological symptoms further. [0003] Factors leading to demyel...

AI Technical Summary

Problems solved by technology

The early treatment is mostly with hormone and nutritional therapy, but the curative effect is difficult to control. Because the disease leads to demyelination and severe neurological damage, secondary axonal damage leads to recurrence, which further aggravates neurological symptoms.

[0003] The factors that lead to demyelinating lesions are complex, and both genetic and environmental factors may contribute to the occurrence of the disease, but the etiology is not fully understood, which also poses difficulties for the improvement of its treatment methods

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