ArticlePsychopharmacology2022
Shanzhiside methylester protects against depression by inhibiting inflammation via the miRNA-155-5p/SOCS1 axis.
Article in Psychopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
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- Bridging Mind and Gut: The Molecular Mechanisms of microRNA, Microbiota, and Cytokine Interactions in Depression.Current gene therapy · 2026Review
- Integrative analysis identifies DCBLD2 and immune-related biomarkers for major depressive disorder: evidence from human peripheral blood, post-mortem brain, and rat models.Frontiers in human neuroscience · 2026Article
- Targeting Inflammation with Natural Products: A Mechanistic Review of Iridoids from Bulgarian Medicinal Plants.Molecules (Basel, Switzerland) · 2025Review
- Pharmacological mechanism of natural antidepressants: the role of epigenetic modifications.Frontiers in pharmacology · 2025Review
- miR-204-5p Plays a Critical Role in the Pathogenesis of Depression and Anti-depression Action of Venlafaxine in the Hippocampus of Mice.Current medicinal chemistry · 2024Article
- Active Fraction of Polyrhachis Vicina Roger (AFPR) Ameliorate Depression Induced Inflammation Response by FTO/miR-221-3p/SOCS1 Axis.Journal of inflammation research · 2023Article
- Distribution profile of iridoid glycosides and phenolic compounds in twoFrontiers in plant science · 2022Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation is a key player in the regulation of depression. Shanzhiside methylester (SM) is an iridoid glycoside with strong anti-inflammatory properties. However, the antidepressant effect of SM remains unknown. The present study aimed to investigate whether SM protects against depression by targeting inflammation. A chronic unpredictable mild stress (CUMS)-induced mouse model of depression was established to assess the antidepressant effect of SM in vivo. In addition, an LPS plus ATP-induced cellular model of inflammation was used to explore the related inflammatory mechanism. We found that both SM and miRNA-155-5p sponge markedly remedied CUMS-induced depression-like behaviors in the sucrose preference test (SPT), tail suspension test (TST), and forced swim test (FST), accompanied by decreased Iba1 expression and the production of TNF-α, IL-1β, and IL-6. Moreover, SM and miRNA-155-5p sponge upregulated the protein levels of SOCS1 and downregulated the protein expression of p-JAK2 and p-STAT3 in the hippocampus of CUMS-exposed mice. miRNA-155-5p expression was also decreased following SM and miRNA-155-5p sponge administration. Furthermore, SM repressed LPS- and ATP-induced inflammatory responses in BV2 cells by regulating the SOCS1/JAK2/STAT3 signaling pathway, which was similar to the anti-inflammatory effects induced by the miRNA-155-5p sponge. Collectively, these findings suggested that SM exerted antidepressant actions by targeting the miRNA-155-5p/SOCS1 axis.
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