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Related Experiment Video

Updated: Jul 27, 2025

Biosynthesis of a Flavonol from a Flavanone by Establishing a One-pot Bienzymatic Cascade

Biosynthesis of a Flavonol from a Flavanone by Establishing a One-pot Bienzymatic Cascade

Published on: August 14, 2019

Flavonoids from

Yi Zheng¹, Xinxiao Lin², Minlan Ren²

¹School of Medicine, Zhejiang University City College, Hangzhou 310015, China. zhengyi_1779819759@163.com.

Zhejiang Da Xue Xue Bao. Yi Xue Ban = Journal of Zhejiang University. Medical Sciences

|June 7, 2023

Summary

This summary is machine-generated.

Total flavonoids from Citrus paradise cv. Changshan-huyou extract (TFC) protect neurons from oxygen-glucose deprivation and reduce chronic cerebral injury in mice. TFC treatment improved cognitive function and neuronal structure by modulating the RhoA-ROCK2 pathway.

Keywords:

Chronic cerebral ischemia Citrus paradise cv. Changshan- huyou Flavonoids Mice Oxygen-glucose deprivation RhoA-ROCK2 signaling pathway

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Area of Science:

Neuroscience
Pharmacology
Biochemistry

Background:

Cerebral ischemia can lead to neuronal damage and cognitive deficits.
Total flavonoids from Citrus paradise cv. Changshan-huyou (TFC) are investigated for neuroprotective properties.

Purpose of the Study:

To evaluate the protective effects of TFC against oxygen-glucose deprivation (OGD) in primary neurons.
To investigate the efficacy of TFC in a mouse model of chronic cerebral ischemia.

Main Methods:

Primary hippocampal neurons were subjected to OGD and treated with varying TFC concentrations.
A chronic cerebral ischemia model was established in mice, followed by TFC treatment and behavioral/histological assessments.
Western blotting was used to analyze key proteins in the RhoA-ROCK2 signaling pathway and actin dynamics.

Main Results:

TFC treatment reversed OGD-induced neurite injury in primary neurons.
TFC administration significantly improved cognitive function and reduced neuronal degeneration in ischemic mice.
TFC modulated the RhoA-ROCK2 pathway, decreasing ROCK2 phosphorylation and increasing LIMK1 and cofilin phosphorylation, while altering G-actin/F-actin ratios.

Conclusions:

TFC exhibits neuroprotective effects against ischemia-induced damage.
TFC ameliorates chronic cerebral injury by preserving cytoskeletal integrity and neuronal structure via the RhoA-ROCK2 pathway.
TFC shows potential as a therapeutic agent for chronic ischemic cerebral injury.