ArticleAlpha psychiatry2025
The Matrine Derivative MASM Alleviates LPS-Induced Depressive-Like Behavior in Mice by Modulating Hippocampal Inflammation, Oxidative Stress, and Autophagy.
Article in Alpha psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Matrine as a multi-disease regulator of ferroptosis: mechanisms, therapeutic applications, and toxicity management.Frontiers in pharmacology · 2026Review
- Exploring potential value of neutrophil extracellular traps in major depressive disorder.Frontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Previous studies have demonstrated a significant association between neuroinflammation and major depressive disorder (MDD). (6aS,10S,11aR,11bR,11cS)-10-methylamino-dodecahydro-3a,7a-diaza-benzo(de)anthracene-8-thione (MASM), a derivative of matrine, has recently been shown to display anti-inflammatory properties. However, its effects on lipopolysaccharide (LPS)-induced depression and the underlying mechanisms remain unexplored. This study aimed to assess the effects of MASM on depressive-like behaviors induced by LPS and to investigate the potential mechanisms involved. Methods: Following intraperitoneal injection of LPS (0.83 mg/kg), MASM was administered. Depressive-like behaviors were assessed through the forced swim test (FST) and tail suspension test (TST). To further explore the mechanisms, LPS-induced BV2 microglial cell models were established. Enzyme-linked immunosorbent assay (ELISA) was used to quantify the expression of TNF-α and high mobility group box 1 (HMGB1), while immunoblotting was performed to assess heme oxygenase-1 (HO-1), sirtuin 1 (SIRT-1), p62, and microtubule-associated protein 1A/1B-light chain 3-phosphatidylethanolamine conjugate (LC3-II) expression. Reactive oxygen species (ROS) levels were evaluated using flow cytometry. Results: MASM pretreatment markedly ameliorated acute depressive-like behaviors in LPS-treated mice and upregulated HO-1 expression in the hippocampus. In LPS-stimulated BV2 cells, MASM reduced the levels of proinflammatory markers TNF-α and HMGB1. Furthermore, MASM mitigated LPS-induced oxidative stress, as evidenced by increased ATP, HO-1, and SIRT-1 levels, along with decreased ROS levels. MASM also restored autophagic function, demonstrated by increased LC3-II expression and reduced p62 levels. Conclusion: These findings suggests that MASM alleviates LPS-induced neuroinflammation and acute depressive-like behaviors, possibly by reducing oxidative stress and promoting autophagy.
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Registered trials
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