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Mirtazapine prevents cell activation, inflammation, and oxidative stress against isoflurane exposure in microglia
1Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, Hebei, China.
Abstract:
Mirtazapine is an antidepressant drug that has been proven to possess a cognitive enhancer efficiency. In this study, we evaluated the potential protective effects of mirtazapine on BV2 microglia in response to isoflurane exposure. Our results show that mirtazapine attenuated isoflurane-induced expression of microglia-specific protein Iba1 in BV2 microglia. Mirtazapine prevented isoflurane-induced production of the pro-inflammatory factors interleukin (IL)-1β and IL-18 by inhibiting the activation of the nod-like receptor family protein 3 (NLRP3) inflammasome in BV2 microglia. The increased reactive oxygen species (ROS) production and elevated expression level of NADPH oxidase 4 (NOX4) in isoflurane-induced BV2 microglia were mitigated by mirtazapine. Isoflurane exposure reduced triggering receptor expressed on myeloid cells 2 (TREM2) expression in BV2 microglia, which was restored by mirtazapine. Moreover, silencing of TREM2 abolished the inhibitory effects of mirtazapine on ionized calcium-binding adapter molecule 1 (Iba1) expression and inflammation in BV2 microglia. From these results, we could infer that mirtazapine exerted a protective effect on BV2 microglia against isoflurane exposure-caused microglia activation, neuroinflammation, and oxidative stress via inducing TREM2 activation. Hence, mirtazapine might be a potential intervention strategy to prevent isoflurane exposure-caused cognitive dysfunction in clinical practice.
Insights
Mirtazapine protects BV2 microglia from isoflurane damage by reducing inflammation and oxidative stress. This neuroprotective effect is mediated through triggering receptor expressed on myeloid cells 2 (TREM2) activation.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Mirtazapine, an antidepressant, shows cognitive-enhancing properties.
- Anesthetic agents like isoflurane can induce neuroinflammation and cognitive dysfunction.
- Microglia play a crucial role in neuroinflammation and are affected by anesthetics.
Purpose of the Study:
- To investigate the protective effects of mirtazapine against isoflurane-induced damage in BV2 microglia.
- To elucidate the underlying mechanisms of mirtazapine's action, focusing on TREM2 signaling.
Main Methods:
- BV2 microglia were exposed to isoflurane.
- Mirtazapine's effects on microglia activation markers (Iba1), inflammatory cytokines (IL-1β, IL-18), NLRP3 inflammasome, ROS production, NOX4 expression, and TREM2 expression were assessed.
- TREM2 was silenced to confirm its role in mirtazapine's protective effects.
Main Results:
- Mirtazapine attenuated isoflurane-induced Iba1 expression and pro-inflammatory cytokine production.
- Mirtazapine inhibited NLRP3 inflammasome activation, reduced ROS production, and decreased NOX4 expression.
- Mirtazapine restored isoflurane-induced reduction in TREM2 expression, and TREM2 silencing abolished mirtazapine's protective effects.
Conclusions:
- Mirtazapine protects BV2 microglia from isoflurane-induced activation, neuroinflammation, and oxidative stress.
- The protective mechanism involves the induction of TREM2 activation.
- Mirtazapine represents a potential therapeutic strategy against isoflurane-induced cognitive dysfunction.
