ArticlePharmaceuticals (Basel, Switzerland)2024
A Selective Nuclear Factor-κB Inhibitor, JSH-23, Exhibits Antidepressant-like Effects and Reduces Brain Inflammation in Rats.
Article in Pharmaceuticals (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Hirudin Attenuates Uric Acid-Induced Renal Tubular Injury via TNFRSF6B-Mediated Suppression of NF-κB Signaling.Pharmacology research & perspectives · 2026Article
- NF‑κB signaling drives Th17‑mediated lacrimal gland injury and tear dysfunction in a murine model of primary Sjögren's syndrome.Molecular medicine reports · 2026Article
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3 authors.
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Abstract
backgroundAccumulating evidence suggests that nuclear factor (NF)-κB is involved in the pathophysiology of mood disorders. OBJECTIVES AND
methodsWe conducted two experimental protocols in rats to investigate the effects of a selective NF-κB inhibitor (JSH-23) on (i) lipopolysaccharide (LPS)-induced inflammation and (ii) on behavioral phenotypes in rat models of depression (sucrose consumption test and forced swim test) and mania (amphetamine-induced hyperactivity test). Additionally, we tested the effects of JSH-23 on levels of inflammatory components (interleukin-6, prostaglandin E2, nuclear phospho-p65, and tumor necrosis factor-α) in the brain.
resultsAcute treatment with JSH-23 (10 mg/kg, intraperitoneally [ip]) led to potent anti-inflammatory effects in LPS-treated rats, including a diminished hypothermic response to LPS and a reduction in pro-inflammatory mediators' levels in the brain. Chronic treatment with JSH-23 (3 mg/kg, ip, once daily, for 14 days) resulted in robust antidepressant-like effects (increased sucrose consumption and decreased immobility time). The antidepressant-like effects of JSH-23 were mostly accompanied by a reduction in levels of pro-inflammatory mediators in the brain. On the other hand, JSH-23 did not reduce amphetamine-induced hyperactivity.
conclusionsAltogether, these data suggest that NF-κB may be a potential therapeutic target for pharmacological interventions for depression.
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