Establishment and intervention strategy of working memory impairment model caused by prefrontal lobe ischemia

By injecting ET-1 into the prefrontal cortex of mice, and using NBP for treatment, the working memory damage caused by prefrontal ischemia was solved, and the effect of protecting cerebral white matter and reducing oligodendrocyte loss and ferrodestruction cell death was achieved.

CN119817527APending Publication Date: 2025-04-15CAPITAL UNIVERSITY OF MEDICAL SCIENCES
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Patent Information

Application Number
CN202510025220.8
Authority / Receiving Office
CN · China
Patent Type
Applications(China)
Current Assignee / Owner
Filing Date
2025-01-07
Publication Date
2025-04-15

AI Technical Summary

Technical Problem

There is currently no effective treatment for working memory damage caused by prefrontal ischemia, and its mechanism is not completely clear, especially whether oligodendrocyte ferrodynamic death directly leads to this injury.

Method used

The effect of its treatment on working memory damage caused by prefrontal ischemia was detected by microinjection of endothelin-1 (ET-1) in the prefrontal cortex region of mice, and treated with phthalide (NBP).

Benefits of technology

Experimental results show that NBP can alleviate working memory damage caused by prefrontal ischemia caused by ET-1, protect the integrity of cerebral white matter, and reduce the loss of oligodendrocytes and iron death.

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Abstract

The invention belongs to the field of medicines and application thereof, and particularly relates to establishment of a working memory impairment model and evaluation of the treatment effect of butylphthalide on working memory impairment caused by prefrontal cortex ischemia. The model is an animal model for working memory impairment caused by prefrontal cortex (mPFC) ischemia caused by endothelin (ET-1), and an intervention measure is butylphthalide medicine. By detecting related indexes of T maze, Y maze, white matter integrity, oligodendroglia cells (OLs) and ferroptosis of a mouse, it is evaluated that a model of working memory impairment caused by mPFC ischemia caused by ET-1 is established, and after the mouse is treated with butylphthalide, the working memory impairment of the mouse is improved, the white matter integrity is enhanced, and the OLs ferroptosis condition is reduced.
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