ArticleJournal of thoracic disease2025
Protective effects of estradiol on neuroinflammation in chronic obstructive pulmonary disease related depression.
Article in Journal of thoracic disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Genetic and Molecular Interconnections Between Chronic Obstructive Pulmonary Disease and Osteoporosis: Insights from Single-Cell and Mendelian Randomization Analyses.International journal of chronic obstructive pulmonary disease · 2026Article
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Authors and funding
9 authors.
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Abstract
Background: Depression among women with chronic obstructive pulmonary disease (COPD) has garnered significant attention. The role of estradiol (E2) on COPD-related depression is unknown. Therefore, this study aimed to investigate the role and underlying mechanism of E2 in COPD related depression. Methods: Female and ovariectomized (OVX) Sprague-Dawley rats (SD rats) were exposed to cigarette smoke (CS) to establish a COPD model. At the end of the experiment, behavioral tests to assess behavioral alterations were tested, pulmonary functions were measured, lung and brain tissue were observed for pathological change. Additionally, we evaluated the levels of oxidative stress and inflammation-related proteins of brain tissue. Results: COPD rats exhibited depression-like behavior, accompanied by a significant decrease in 5-hydroxytryptamine (5-HT) levels in the plasma and cerebral cortex. The combination of OVX and CS exposure resulted in a rat model of COPD-related depression. In this model, brain microglia and astrocytes were activated, with increased expression of nuclear factor erythroid 2-related factor-2 (Nrf2), quinone oxidoreductase 1 (NQO1), heme-oxygenase-1 (HO1), and phosphorylated nuclear factor kappa B (p-NFκB) proteins, alongside enhanced M1 polarization in microglia. These changes were correlated with the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun-N-terminal kinase (JNK). Conclusions: Our findings indicate that E2 protects against depression-like behavior induced by CS, which may be related to the activation of microglia and M1 polarization through the ERK1/2 and JNK pathways. Furthermore, estrogen levels appear to play a crucial role in the anti-neuroinflammatory processes associated with the onset and progression of depression in COPD.
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