Engineered exosome prepared by loading calycosin into astragalus membranaceus exosome and preparation method and application thereof

CN122140652APending Publication Date: 2026-06-05SHANXI UNIV OF CHINESE MEDICINE
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Patent Information

Authority / Receiving Office
CN · China
Patent Type
Applications(China)
Current Assignee / Owner
SHANXI UNIV OF CHINESE MEDICINE
Filing Date
2026-02-13
Publication Date
2026-06-05

AI Technical Summary

Technical Problem

Verbena isoflavones have poor water solubility, making it difficult to cross the blood-brain barrier and resulting in low bioavailability, which limits their application in the treatment of Parkinson's disease.

Method used

Astragalus exosomes were used as carriers to load verbascoside isoflavones via a co-incubation method to prepare engineered exosomes (AS-Exos-CA). The blood-brain barrier penetration ability of astragalus exosomes was utilized to deliver verbascoside isoflavones into the brain for targeted enrichment.

Benefits of technology

Improving the bioavailability of verbascoside in brain tissue and significantly enhancing its antioxidant, anti-inflammatory, and neuroprotective effects through the synergistic effect of carriers and drugs, it is superior to the use of verbascoside or astragalus exosomes alone, providing a comprehensive therapeutic effect for Parkinson's disease.

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Abstract

The application provides an engineered exosome prepared from Astragalus membranaceus exosome loaded with calycosin and a preparation method and application thereof. Astragalus membranaceus exosome is used as a carrier, and calycosin is loaded through co-incubation to obtain the engineered exosome. The system has a particle size of about 100-200 nm, maintains a typical double-membrane structure, and realizes high drug loading rate and good stability. In vitro experiments show that AS-Exos-CA can be efficiently taken up by PC12 and other neuron-like cells; DiR labeling and in vivo imaging results confirm that AS-Exos-CA can cross the blood-brain barrier of mice and be enriched in brain tissues. Research on a PC12 cell model damaged by MPP+ and a Parkinson's disease mouse model induced by MPTP shows that AS-Exos-CA can significantly improve cell survival rate and mouse motor function, reduce the loss of dopaminergic neurons in the substantia nigra, activate the Nrf2 / System Xc- / GPX4 antioxidant pathway, reduce the levels of Fe2+, MDA and ROS and increase GSH, reduce mitochondrial damage and inhibit ferroptosis. Compared with the use of CA or AS-Exos alone, the system has better neuroprotective and anti-Parkinson's treatment effects.
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