TL;DR
Mechanistically, CPE activated the BDNF/Nrf2 axis, increased GPX4 activity, suppressed acyl-CoA synthetase long chain family member 4 expression, and reduced iron accumulation, and all protective effects of CPE overexpression were reversed by ML385.
MC1R-related signaling in the PFC is highlighted as an important contributor to inflammation-associated depression and NDP-MSH alleviates inflammation-associated depressive-like behaviors in association with melanocortin signaling involving MC1R and downstream cAMP/PKA activation.
The SIRT1/NF-κB pathway is highlighted as a key mechanism mediating the therapeutic effect of THC against depression by activating SIRT1 to suppress NF‑κB-mediated neuroinflammation and restore neurotrophic factor expressions.
Depression is a highly prevalent affective disorder, and current pharmacotherapies are often limited by suboptimal efficacy and adverse effects. Diosmetin, a dietary flavonoid, exhibits neuroprotective properties through antioxidant and anti-inflammatory mechanisms; however, its antidepressant potential remains insuffi...
The role of ferroptosis is revealed in the T2DD model and provides new insights into therapeutic interventions targeting lipid metabolism pathways.
UB alleviates CUMS-induced depressive-like behavior and hippocampal neuronal damage by upregulating SLP2 and regulating the PINK1/Parkin-mediated mitophagy pathway and presents a new potential target and theoretical basis for developing natural compound-based therapies for depression.
LIM ameliorates HUA-induced cognitive impairment by suppressing microglial activation and neuroinflammation, which is associated with the inhibition of the HIF-1α/iNOS signaling pathway, underscoring its therapeutic potential.
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