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miR-92b-3p Exerts Neuroprotective Effects on Ischemia/Reperfusion-Induced Cerebral Injury via Targeting NOX4 in a Rat
Yongpan Huang1, Jiayu Tang2, Xiaojuan Li2
1School of Medicine, Changsha Social Work College, Changsha, Hunan, China.
Abstract:
The necessity to increase the efficiency of organ preservation has pushed researchers to consider the mechanisms to minimize cerebral ischemia/reperfusion (I/R) injury. Hence, we evaluated the role of the miR-92b-3p/NOX4 pathway in cerebral I/R injury. A cerebral I/R injury model was established by blocking the left middle cerebral artery for 2 h and reperfusion for 24 h, and a hypoxia/reoxygenation (H/R) model was established. Thereafter, cerebral I/R increased obvious neurobiological function and brain injury (such as cerebral infarction, apoptosis, and cell morphology changes). In addition, we noted a significant decrease in the expression of miR-92b-3p, as well as increases in apoptosis and oxidative stress and an increase in NOX4. Furthermore, overexpression of miR-92b-3p blocked the inhibitory effect of miR-92b-3p on the expression of NOX4 and the accumulation of oxygen-free radicals. Bioinformatics analysis found that NOX4 may be the target gene regulated by miR-92b-3p. In conclusion, the involvement of the miR-92b-3p/NOX4 pathway ameliorated cerebral I/R injury through the prevention of apoptosis and oxidative stress. The miR-92b-3p/NOX4 pathway could be considered a potential therapeutic target to alleviate cerebral I/R injury.
Insights
Researchers explored the miR-92b-3p/NOX4 pathway to reduce brain injury from cerebral ischemia/reperfusion (I/R). Findings show this pathway can prevent apoptosis and oxidative stress, offering a potential therapeutic target for I/R injury.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- Cerebral ischemia/reperfusion (I/R) injury poses a significant challenge in organ preservation and neurological recovery.
- Understanding the molecular mechanisms underlying I/R injury is crucial for developing effective therapeutic strategies.
Purpose of the Study:
- To investigate the role of the miR-92b-3p/NOX4 pathway in the pathogenesis of cerebral I/R injury.
- To determine if modulating this pathway can mitigate neuronal damage and improve outcomes after I/R events.
Main Methods:
- Establishment of a rodent model of cerebral I/R injury by middle cerebral artery occlusion and reperfusion.
- In vitro hypoxia/reoxygenation (H/R) model to study cellular responses.
- Assessment of neurobiological function, brain infarction, apoptosis, and cell morphology.
- Quantitative analysis of miR-92b-3p and NOX4 expression levels.
- Bioinformatics analysis to predict the regulatory relationship between miR-92b-3p and NOX4.
Main Results:
- Cerebral I/R significantly impaired neurobiological function, increased brain infarction, apoptosis, and altered cell morphology.
- Expression of miR-92b-3p was significantly decreased, while NOX4 expression, apoptosis, and oxidative stress were elevated post-I/R.
- Overexpression of miR-92b-3p counteracted the detrimental effects of I/R by inhibiting NOX4 expression and reducing oxidative stress.
- Bioinformatics analysis suggested NOX4 as a direct target gene of miR-92b-3p.
Conclusions:
- The miR-92b-3p/NOX4 pathway plays a critical role in modulating cerebral I/R injury.
- Activation of this pathway, specifically by upregulating miR-92b-3p, ameliorates I/R-induced apoptosis and oxidative stress.
- The miR-92b-3p/NOX4 axis represents a promising therapeutic target for alleviating cerebral I/R injury.
