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Agomelatine Attenuates Isoflurane-Induced Inflammation and Damage in Brain Endothelial Cells
Fang Cheng1, Huanxian Chang2, Fengfeng Yan1
1Department of Anesthesiology and Pain Clinic, The Affiliated Lianyungang Oriental Hospital of Xuzhou Medical University.
Background And Purpose:
Neurotoxicity of anesthetics has been widely observed by clinicians. It is reported that inflammation and oxidative stress are involved in the pathological process. In the present study, we aimed to assess the therapeutic effects of agomelatine against isoflurane-induced inflammation and damage to brain endothelial cells.
Materials And Methods:
MTT assay was used to detect cell viability in order to determine the optimized concentration of agomelatine. The bEnd.3 brain endothelial cells were treated with 2% isoflurane in the presence or absence of agomelatine (5, 10 μM) for 24 h. LDH release was evaluated and the ROS levels were checked using DHE staining assay. The expressions of IL-6, IL-8, TNF-α, VEGF, TF, VCAM-1, and ICAM-1 were evaluated using real-time PCR and ELISA. Real-time PCR and Western blot analysis were used to determine the expression level of Egr-1.
Results:
The decreased cell viability promoted LDH release and elevated ROS levels induced by isoflurane were significantly reversed by the introduction of agomelatine in a dose-dependent manner. The expression levels of IL-6, IL-8, TNF-α, VEGF, TF, VCAM-1, and ICAM-1 were elevated by stimulation with isoflurane, which were significantly suppressed by the administration of agomelatine. The up-regulation of transcriptional factor Egr-1 induced by isoflurane was down-regulated by agomelatine.
Conclusion:
Agomelatine might attenuate isoflurane-induced inflammation and damage via down-regulating Egr-1 in brain endothelial cells.
Insights
Agomelatine protects brain endothelial cells from isoflurane-induced damage. It reduces inflammation and oxidative stress by down-regulating Egr-1, offering a potential therapeutic strategy.
Area of Science:
- Neuroscience
- Pharmacology
- Cell Biology
Background:
- Anesthetic neurotoxicity is a clinical concern.
- Inflammation and oxidative stress contribute to anesthetic-induced brain damage.
- Agomelatine's therapeutic potential against anesthetic effects requires investigation.
Purpose of the Study:
- To evaluate agomelatine's protective effects on brain endothelial cells against isoflurane-induced inflammation and damage.
- To investigate the underlying molecular mechanisms, including Egr-1 regulation.
Main Methods:
- Primary bEnd.3 brain endothelial cells were exposed to isoflurane with or without agomelatine.
- Cell viability (MTT assay), LDH release, and reactive oxygen species (ROS) levels were measured.
- Gene and protein expression of inflammatory markers (IL-6, IL-8, TNF-α, VEGF, TF, VCAM-1, ICAM-1) and Egr-1 were analyzed via real-time PCR and Western blot.
Main Results:
- Agomelatine reversed isoflurane-induced decreases in cell viability, elevated LDH release, and increased ROS levels in a dose-dependent manner.
- Agomelatine significantly suppressed the isoflurane-induced upregulation of inflammatory markers and VEGF.
- Agomelatine downregulated the expression of the transcriptional factor Egr-1, which was upregulated by isoflurane.
Conclusions:
- Agomelatine demonstrates protective effects against isoflurane-induced neuroinflammation and endothelial cell damage.
- The mechanism involves the downregulation of Egr-1 expression.
- Agomelatine represents a potential therapeutic agent for mitigating anesthetic-induced brain injury.
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