Psychiatry research · 2026
Aldolase C and T helper 1 polarization in postpartum depression: a novel perspective on disease mechanisms.
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Du Zhixin, Fan Pengbei, Fan Yazhe, Wang Yueyang, Yang Liping, Hou Junlin
Аннотация
PURPOSE: Postpartum depression (PPD) is common, yet its pathophysiology remains unclear and reliable early biomarkers are lacking.
METHODS: Mendelian randomization, bioinformatics analyses, and animal experiments were integrated. A prenatal stress-induced rat model of PPD was established. Depressive-like behaviors were assessed using the open field and forced swim tests, and brain histopathology was examined by hematoxylin-eosin staining. Serum HPA-axis hormones, ALDOC, lactic acid, and Th1/Th2 cytokines were measured by ELISA. ALDOC was analyzed by Western blot. T-bet and GATA3 mRNA expression in peripheral blood mononuclear cells was detected by qRT-PCR, and the T-bet/GATA3 ratio was calculated.
RESULTS: Sixteen overlapping genes were identified, suggesting the involvement of Th cells in PPD and highlighting ALDOC as a potential candidate biomarker associated with Th1-related immune alterations. PPD rats showed depressive-like behaviors and HPA-axis activation, with increased CRH and ACTH but unchanged CORT levels. ALDOC and lactic acid levels were significantly increased, accompanied by elevated Th1-related cytokines (IFN-γ, TNF-α, and IL-1β) and an increased IFN-γ/IL-4 ratio, whereas Th2-related cytokines showed no significant changes. Consistently, T-bet expression increased, GATA3 expression decreased, and the T-bet/GATA3 ratio was elevated, further supporting a possible Th1-skewed immune response. Brain histopathology showed cellular damage and reduced cell density. In the PFC, ALDOC upregulation was accompanied by increased pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α), which may suggest coordinated central neuroinflammation and peripheral immune imbalance.
CONCLUSIONS: ALDOC may contribute to PPD pathogenesis by promoting Th1 polarization and inflammatory activation.
METHODS: Mendelian randomization, bioinformatics analyses, and animal experiments were integrated. A prenatal stress-induced rat model of PPD was established. Depressive-like behaviors were assessed using the open field and forced swim tests, and brain histopathology was examined by hematoxylin-eosin staining. Serum HPA-axis hormones, ALDOC, lactic acid, and Th1/Th2 cytokines were measured by ELISA. ALDOC was analyzed by Western blot. T-bet and GATA3 mRNA expression in peripheral blood mononuclear cells was detected by qRT-PCR, and the T-bet/GATA3 ratio was calculated.
RESULTS: Sixteen overlapping genes were identified, suggesting the involvement of Th cells in PPD and highlighting ALDOC as a potential candidate biomarker associated with Th1-related immune alterations. PPD rats showed depressive-like behaviors and HPA-axis activation, with increased CRH and ACTH but unchanged CORT levels. ALDOC and lactic acid levels were significantly increased, accompanied by elevated Th1-related cytokines (IFN-γ, TNF-α, and IL-1β) and an increased IFN-γ/IL-4 ratio, whereas Th2-related cytokines showed no significant changes. Consistently, T-bet expression increased, GATA3 expression decreased, and the T-bet/GATA3 ratio was elevated, further supporting a possible Th1-skewed immune response. Brain histopathology showed cellular damage and reduced cell density. In the PFC, ALDOC upregulation was accompanied by increased pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α), which may suggest coordinated central neuroinflammation and peripheral immune imbalance.
CONCLUSIONS: ALDOC may contribute to PPD pathogenesis by promoting Th1 polarization and inflammatory activation.