Title:The Protective Effect of Vitexin Compound B-1 on Rat Cerebral I/R
Injury through a Mechanism Involving Modulation of miR-92b/NOX4
Pathway
Volume: 22
Issue: 1
Author(s): Zhong-Yang Hu, Zhong-Bao Yang, Ruxu Zhang, Xiu-Ju Luo*Jun Peng*
Affiliation:
- Department of Laboratory Medicine, The Third Xiangya Hospital of Central South University,
Changsha 410013, China
- Department of Pharmacology, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha
410078, China
Keywords:
Ischemic stroke, ischemia/reperfusion injury, miR-92b, NADPH oxidase, vitexin compound B-1, cerebral injury.
Abstract:
Background: Recent studies have uncovered that vitexin compound B-1 (VB-1) can protect
neurons against hypoxia/reoxygenation (H/R)-induced oxidative injury through suppressing NOX4
expression.
Objective: The aims of this study are to investigate whether VB-1 can protect the rat brain against ischemia/
reperfusion (I/R) injury and whether its effect on NOX4 expression is related to modulation of
certain miRNAs expression.
Methods: Rats were subjected to 2 h of cerebral ischemia followed by 24 h of reperfusion to establish
an I/R injury model, which showed an increase in neurological deficit score and infarct volume concomitant
with an upregulation of NOX4 expression, increase in NOX activity, and downregulation of
miR-92b.
Results: Administration of VB-1 reduced I/R cerebral injury accompanied by a reverse in NOX4 and
miR-92b expression. Similar results were achieved in a neuron H/R injury model. Next, we evaluated
the association of miR-92b with NOX4 by its mimics in the H/R model. H/R treatment increased neurons
apoptosis concomitant with an upregulation of NOX4 and NOX activity while downregulation of
miR-92b. All these effects were reversed in the presence of miR-92b mimics, confirming the function
of miR-92b in suppressing NOX4 expression.
Conclusion: We conclude the protective effect of VB-1 against rat cerebral I/R injury through a
mechanism involving modulation of miR-92b/NOX4 pathway.
