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Updated: Feb 5, 2026

A Low Mortality Rat Model to Assess Delayed Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage
Published on: January 17, 2013
MiR-7 alleviates secondary inflammatory response of microglia caused by cerebral hemorrhage through inhibiting TLR4
1Department of Cerebral Surgery, The First People's Hospital of Jiande, Jiande, China. 272580203@qq.com.
Objective:
This study was conducted to analyze the effect of miR-7 on the inflammatory response of microglia in vitro and in vivo by constructing an intracerebral hemorrhage model.
Patients And Methods:
In this study, we first established a model of cerebral hemorrhage in rat for in vivo experiments, and used lipoprotein (LPS) to induce an inflammatory response development in microglial cells, and constructed microglial inflammation models for in vitro experiments. Quantitative Real-time-polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-7 in the rat model of cerebral hemorrhage and microglia with inflammation. The effect of miR-7 on the inflammation caused by intracerebral hemorrhage was evaluated through measuring the expression of IL-1β, IL-8 and TNF-α by enzyme-linked immunosorbent assay (ELISA). Dual luciferase reporter assay was used to detect the binding site of miR-7 to TLR4. Western blot was used to evaluate the level of TLR4 after overexpression and knockdown of miR-7 and to evaluate whether miR-7 alleviated the secondary inflammatory response of microglia after cerebral hemorrhage by inhibiting the expression of TLR4.
Results:
The expression of miR-7 in the rat cerebral hemorrhage model and microglial inflammation model tissue was significantly lower than that in the normal control group. Expression of inflammatory cytokines including IL-1β, IL-8 and TNF-α was significantly increased in rats with intracerebral hemorrhage and microglial inflammation in rats, and the expression of these inflammatory cytokines was partially reversed after overexpression of miR-7. Double luciferase reporter gene and ELISA results showed that miR-7 could inhibit the expression of TLR4 and relieve the secondary inflammatory response of microglia after cerebral hemorrhage.
Conclusions:
We demonstrated that, in in vivo and in vitro experiments, miR-7 could reduce the LPS-induced inflammatory response produced by microglial cells, and alleviate the inflammation in the brain of rats with cerebral hemorrhage.
Insights
MicroRNA-7 (miR-7) plays a crucial role in mitigating neuroinflammation following intracerebral hemorrhage. This study demonstrates that miR-7 reduces inflammatory responses in microglia, offering a potential therapeutic target for brain injury.
Area of Science:
- Neuroscience
- Molecular Biology
- Immunology
Background:
- Microglia play a central role in neuroinflammation, particularly after events like intracerebral hemorrhage (ICH).
- Dysregulation of microRNAs (miRNAs) is implicated in inflammatory processes within the central nervous system.
Purpose of the Study:
- To investigate the role of microRNA-7 (miR-7) in regulating microglial inflammatory responses in vitro and in vivo.
- To determine if miR-7 can alleviate neuroinflammation associated with an intracerebral hemorrhage model.
Main Methods:
- Established rat models for in vivo ICH and lipopolysaccharide (LPS)-induced microglial inflammation in vitro.
- Utilized quantitative real-time polymerase chain reaction (qRT-PCR) to measure miR-7 expression.
- Assessed inflammatory cytokines (IL-1β, IL-8, TNF-α) via enzyme-linked immunosorbent assay (ELISA).
- Employed dual luciferase reporter assays and Western blot to analyze miR-7's interaction with Toll-like receptor 4 (TLR4).
Main Results:
- miR-7 expression was significantly downregulated in both ICH and microglial inflammation models.
- Overexpression of miR-7 partially reversed the increased expression of inflammatory cytokines (IL-1β, IL-8, TNF-α).
- miR-7 was found to inhibit TLR4 expression, thereby reducing microglial inflammatory responses.
Conclusions:
- miR-7 exhibits a protective effect against neuroinflammation by suppressing microglial activation.
- Restoring miR-7 levels can alleviate inflammation in the brain following intracerebral hemorrhage.
- Targeting miR-7 represents a potential therapeutic strategy for managing ICH-induced neuroinflammation.
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