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Published on: September 24, 2020
Sevoflurane prevents miR-181a-induced cerebral ischemia/reperfusion injury
Yanan Zhang1, Zhengzheng Shan2, Yanling Zhao1
1Department of Anesthesiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450000, China.
Background:
Sevoflurane (sevo) has been reported to be an effective neuroprotective agent in cerebral ischemia/reperfusion injury (CIRI). However, the precise molecular mechanism underlying sevo preconditioning in CIRI remains largely unknown.
Methods:
A middle cerebral artery occlusion (MCAO) rat model and primary cortical neurons after oxygen-glucose deprivation and reoxygenation (OGDR) were used as the in vivo and in vitro models of CIRI. The expression profiles of miR-181a and X chromosome-linked inhibitor-of-apoptosis protein (XIAP) in the cerebral cortex of rats and in cortical neurons were examined by qRT-PCR and Western blot, respectively. The infarct volumes were measured by TTC staining and neurological deficits in rats was determined by Zea-Longa scoring criteria. The cell viability, lactate dehydrogenase (LDH) release and apoptotic rate were detected in cortical neurons by MTT assay, LDH analysis and flow cytometry. Western blot analysis was performed to assess the expression of apoptosis-related protein. Luciferase reporter assay was used to confirm the interaction between miR-181a and XIAP.
Results:
miR-181a was upregulated and XIAP was downregulated in rats after MCAO. Sevo preconditioning attenuated miR-181a expression and promoted XIAP level in a rat model of CIRI. Sevo preconditioning ameliorated anti-miR-181a-mediated protective effects on cerebral ischemia in rat model of CIRI, presented as the decrease of infarct volume, neurological deficit and apoptosis. Moreover, sevo pretreatment abated miR-181a-induced cellular injury in primary cortical neurons after OGD, embodied by the increase of cell viability, the reduction of LDH release and the decline of apoptosis. Furthermore, miR-181a suppressed XIAP expression by binding to its 3'UTR in cortical neurons, and sevo-mediated increase on XIAP expression was counteracted by miR-181 overexpression in OGDR-treated neurons.
Conclusion:
Sevo preconditioning protected against CIRI in vitro and in vivo possibly by inhibiting miR-181a and facilitating XIAP.
Insights
Sevoflurane preconditioning protects against cerebral ischemia/reperfusion injury by inhibiting miR-181a and increasing XIAP. This study elucidates the molecular mechanism of sevoflurane neuroprotection in CIRI models.
Area of Science:
- Neuroscience
- Anesthesiology
- Molecular Biology
Background:
- Sevoflurane is a known neuroprotective agent against cerebral ischemia/reperfusion injury (CIRI).
- The precise molecular mechanisms underlying sevoflurane's neuroprotective effects in CIRI are not fully understood.
Purpose of the Study:
- To investigate the molecular mechanism of sevoflurane preconditioning in protecting against CIRI.
- To examine the roles of miR-181a and X chromosome-linked inhibitor-of-apoptosis protein (XIAP) in sevoflurane-mediated neuroprotection.
Main Methods:
- Established in vivo (MCAO rat model) and in vitro (OGDR cortical neuron model) for CIRI.
- Quantified miR-181a and XIAP expression using qRT-PCR and Western blot.
- Assessed infarct volume, neurological deficits, cell viability, LDH release, and apoptosis.
- Utilized luciferase reporter assays to confirm the interaction between miR-181a and XIAP.
Main Results:
- Sevoflurane preconditioning attenuated miR-181a and upregulated XIAP expression in CIRI models.
- Sevoflurane reduced infarct volume, neurological deficits, and apoptosis in rats.
- In vitro, sevoflurane pretreatment increased neuronal viability and decreased LDH release and apoptosis.
- miR-181a was found to suppress XIAP expression by binding to its 3'UTR.
Conclusions:
- Sevoflurane preconditioning demonstrates neuroprotective effects against CIRI.
- The mechanism involves the inhibition of miR-181a and the facilitation of XIAP expression.
- This study provides key insights into the molecular pathways of sevoflurane-induced neuroprotection.
