Anna Wiktorowska-Owczarek

Department of Pharmacology and Toxicology, Medical University of Lodz, Zeligowskiego 7/9, 90-752 Lodz, Poland.

2 papers in the library · 22 citations · publishing 2025

Papers

Unveiling the Anti-Inflammatory Effects of Antidepressants: A Systematic Review of Human Studies over the Last Decade.

Pharmaceuticals (Basel, Switzerland) June 10, 2025 Layla Bleibel, Paulina Sokołowska, Gabriela Henrykowska et al. 18 citations

Antidepressants like SSRIs, SNRIs, esketamine, and ketamine reduce inflammation in people with depression by lowering pro-inflammatory cytokines or boosting anti-inflammatory cytokines in the blood and brain regions such as the hippocampus and prefrontal cortex. These effects occur through multiple pathways, including NF-κB, the NLRP3 inflammasome, the glutamatergic system, the gut-brain axis, the hypothalamic-pituitary axis, impaired neuroplasticity, and the kynurenine pathway. The findings suggest that anti-inflammatory actions contribute to the therapeutic benefits of these treatments, supporting the link between depression and inflammation.

DOI: 10.3390/ph18060867 Full text Ketamine Snri Ssri Depression-inflammation link +2

Modulation of ER Stress and Inflammation by S-Ketamine, R-Ketamine, and Their Metabolites in Human Microglial Cells: Insights into Novel Targets for Depression Therapy.

Cells June 3, 2025 Marta Jóźwiak-Bębenista, Anna Wiktorowska-Owczarek, Małgorzata Siatkowska et al. 4 citations

Ketamine and its metabolites—including R-ketamine, S-ketamine, and the hydroxynorketamines (2S,6S-HNK and 2R,6R-HNK)—directly reduce markers of endoplasmic reticulum (ER) stress and inflammation in human microglial cells. In cells treated with tunicamycin to induce ER stress, all compounds lowered expression and protein levels of CHOP and GRP78, two key components of the unfolded protein response (UPR). In microglia stimulated with lipopolysaccharide (LPS), the compounds decreased levels of the inflammatory cytokine IL-6 and, to a lesser extent, IL-8. These findings point to a glia-targeted mechanism for modulating ER stress and neuroinflammation, supporting further in vivo research to develop antidepressants with fewer psychoactive side effects than current treatments.

DOI: 10.3390/cells14110831 Full text Treatment-resistant depression Chop Er stress Grp78 +8