Escitalopram's inflammatory effect on the mammalian macrophages and its intracellular mechanism of action

Önal, Harika Topal; Yetkin, Derya; Ayaz, Furkan

doi:10.1016/j.pnpbp.2023.110762

Cited by 9 publications

(2 citation statements)

References 33 publications

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“…Moreover, escitalopram demonstrated a notable elevation in the serum concentrations of the anti-inflammatory cytokine interleukin-10 [ 25 ]. However, it has been reported that escitalopram induced a notable increase in the interleukin-6 and tumor necrosis factor-alpha levels in mammalian macrophage cells [ 26 ]. Hence, further comprehensive investigations are warranted to clarify the impact of escitalopram on the immune system.…”

Section: Discussionmentioning

confidence: 99%

The safety and efficacy of escitalopram and sertraline in post-stroke depression: a randomized controlled trial

Yan,

2024

BMC Psychiatry

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Objectives This study aims to evaluate the safety and efficacy of escitalopram and sertraline in post-stroke depression (PSD) patients, to provide more reliable therapeutics for cardiovascular and psychiatric clinical practice. Methods We recruited 60 patients (aged 40–89 years old) with an ICD-10 diagnosis of PSD, who were then randomly assigned to two groups and treated with flexible doses of escitalopram (10 to 20 mg/day, n = 30) or sertraline (50 to 200 mg/day, n = 30) for consecutive 8 weeks, respectively. The 24-item Hamilton Depression Rating Scale (HAMD-24), the 14-item Hamilton Anxiety Rating Scale (HAMA-14), the Treatment Emergent Symptom Scale (TESS), the Montreal Cognitive Assessment Scale (MOCA), and the Activity of Daily Living scale (ADL) were used to assess patients before, during, and after treatment for depression, anxiety, adverse effects, cognitive function, and daily living activities. Repeated measures ANOVA, the Mann–Whitney U test, the chi-square test (χ2), or Fisher’s exact test was employed to assess baseline demographics, response rate, adverse effects rate, and changes in other clinical variables. Results Significant reduction in HAMD-24 and HAMA-14 scores was evaluated at baseline, as well as 1, 3, 4, 6, and 8 weeks of drug intervention (p < 0.01). There was a significant group difference in post-treatment HAMD-24 scores (p < 0.05), but no difference was observed in HAMA-14 scores (p > 0.05). Further analysis showed a significant variance in the HAMD-24 scores between the two groups at the end of the first week (p < 0.01). The incidence of adverse effects in both patient groups was mild, but there was a statistically significant difference between the two groups (p < 0.05). The improvement in cognitive function and the recovery of daily living abilities were comparable between both groups (p > 0.05). Conclusion Escitalopram and sertraline showed comparable efficacy for anxiety symptoms, cognitive function, and daily living abilities in PSD patients. In addition, escitalopram was more appropriate for alleviating depressive symptoms. To validate the conclusion, trials with a larger sample size are in demand in the future. The registration number is ChiCTR1800017373.

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Section: Discussionmentioning

confidence: 99%

The safety and efficacy of escitalopram and sertraline in post-stroke depression: a randomized controlled trial

Yan,

2024

BMC Psychiatry

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“…Currently, the growth rate of global depressive patients is increasing yearly at a rate of 11.3% (Wang, Ying, et al, 2023). The manifestations of depression are diverse, and its etiology and pathogenesis remain unclear, despite the continuous proposal of new hypotheses over the past 50 years, including the classical monoamine hypothesis, modern monoamine hypothesis, the hypothalamic-pituitary-adrenal axis negative feedback hypothesis and neurotrophic hypothesis (Marinho et al, 2023;Önal et al, 2023). Research has found that serotonin (5-HT) content declines in the brain, and the weakening of 5-HT neurotransmission function is still considered the major pathogenesis of depression (Bartova et al, 2023).…”

Section: Introductionmentioning

confidence: 99%

Atractylenolide I improves behaviors in mice with depression‐like phenotype by modulating neurotransmitter balance via 5‐HT2A

Pei,

Du,

et al. 2023

Phytotherapy Research

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To explore the antidepressant effects and targets of atractylenolide I (ATR) through a network pharmacological approach. Relevant targets of ATR and depression analyzed by network pharmacology were scored (identifying 5‐HT2A targets). Through elevated plus maze, open field, tail suspension, and forced swimming tests, the behavioral changes of mice with depression (chronic unpredictable mild stress [CUMS]) were examined, and the levels of neurotransmitters including serotonin, dopamine, and norepinephrine (5‐HT, DA, and NE) were determined. The binding of ATR to 5‐HT2A was verified by small molecular‐protein docking. ATR improved the behaviors of CUMS mice, elevated their levels of neurotransmitters 5‐HT, DA, and NE, and exerted a protective effect on their nerve cell injury. After 5‐HT2A knockout, ATR failed to further improve the CUMS behaviors. According to the results of small molecular‐protein docking and network pharmacological analysis, ATR acted as an inhibitor by binding to 5‐HT2A. ATR can improve the behaviors and modulate the neurotransmitters of CUMS mice by targeting 5‐HT2A.

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Paroxetine’s effect on the proinflammatory cytokine stimulation and intracellular signaling pathways in J774.2 cells

Önal,

Yetkin,

Ayaz

2023

Naunyn-Schmiedeberg's Arch Pharmacol

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Escitalopram's inflammatory effect on the mammalian macrophages and its intracellular mechanism of action

Cited by 9 publications

References 33 publications

The safety and efficacy of escitalopram and sertraline in post-stroke depression: a randomized controlled trial

The safety and efficacy of escitalopram and sertraline in post-stroke depression: a randomized controlled trial

Atractylenolide I improves behaviors in mice with depression‐like phenotype by modulating neurotransmitter balance via 5‐HT2A

Paroxetine’s effect on the proinflammatory cytokine stimulation and intracellular signaling pathways in J774.2 cells

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