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Updated: Mar 23, 2026
A Rat Model of Middle Cerebral Artery Occlusion/Reperfusion Without Damaging the Anatomical Structure of Cerebral Vessels
Published on: May 17, 2024
Protective effect of microRNA-138 against cerebral ischemia/reperfusion injury in rats
Xiang-Jun Tang1, Ming-Huan Yang1, Gang Cao1
1Department of Neurosurgery, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, P.R. China.
Abstract:
MicroRNAs (miRs) serve a regulatory function in oxidative radical-mediated inflammation and apoptosis during ischemia/reperfusion (IR) injury. Lipocalin 2 (Lcn-2), a target protein of miR-138, is widely involved in the systemic response to IR injury. The aim of the present study was to investigate the association between miR-138 and Lcn-2 in a rat model of cerebral ischemia/reperfusion (CIR) injury and to verify the interaction between miR-138 and Lcn-2 in a PC12 cell model of hypoxia/reoxygenation injury. Reverse transcription-quantitative polymerase chain reaction and western blot analysis were used to detect the mRNA and protein expression levels of miR-138 and Lcn-2. Cell proliferation was determined by MTT assay. The results suggested that the expression of miR-138 was inversely correlated with the expression of Lcn-2 in the CIR rat model and the PC12 cells subjected to hypoxia and reoxygenation. The expression of Lcn-2 was inhibited by miR-138 mimics and enhanced by miR-138 inhibitors, thereby indicating that miR-138 functions as a negative regulator for Lcn-2 expression. This study provides an experimental basis for the further study of miR-138-based therapy for CIR injury.
Insights
MicroRNAs (miRs) regulate inflammation and cell death in ischemia/reperfusion (IR) injury. This study shows miR-138 inhibits Lipocalin 2 (Lcn-2) expression, suggesting a therapeutic target for cerebral IR injury.
Area of Science:
- Biochemistry
- Molecular Biology
- Neuroscience
Background:
- MicroRNAs (miRs) regulate oxidative stress, inflammation, and apoptosis in ischemia/reperfusion (IR) injury.
- Lipocalin 2 (Lcn-2) is implicated in the systemic response to IR injury and is a target of miR-138.
Purpose of the Study:
- To investigate the relationship between miR-138 and Lcn-2 in cerebral ischemia/reperfusion (CIR) injury.
- To validate the interaction between miR-138 and Lcn-2 in a cellular model of hypoxia/reoxygenation.
Main Methods:
- Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blot to assess miR-138 and Lcn-2 expression.
- MTT assay to evaluate cell proliferation.
- In vitro experiments using PC12 cells subjected to hypoxia/reoxygenation.
Main Results:
- miR-138 expression was inversely correlated with Lcn-2 expression in both CIR rat models and PC12 cells.
- miR-138 mimics decreased Lcn-2 expression, while miR-138 inhibitors increased it.
- miR-138 acts as a negative regulator of Lcn-2 expression.
Conclusions:
- miR-138 negatively regulates Lcn-2 expression in the context of CIR injury.
- This interaction provides a potential therapeutic avenue for treating CIR injury.
- Further research into miR-138-based therapies for CIR is warranted.
