ArticleJournal of psychopharmacology (Oxford, England)2021
Isoginkgetin treatment attenuated lipopolysaccharide-induced monoamine neurotransmitter deficiency and depression-like behaviors through downregulating p38/NF-κB signaling pathway and suppressing microglia-induced apoptosis.
Article in Journal of psychopharmacology (Oxford, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 22 citations in OpenAlex.
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- Isoginkgetin protects chondrocytes and inhibits osteoarthritis through NF-κB and P21 signaling pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- Exploring the neuroprotective mechanisms of Jiawei Suanzaoren decoction in depression: insights from network pharmacology and molecular docking.BMC complementary medicine and therapies · 2025Article
- The depression-heart connection: cardiovascular risks in cancer patients from NHANES 2005-2018.BMC psychiatry · 2025Article
- Exosomes Derived from DPA-treated UCMSCs Attenuated Depression-like Behaviors and Neuroinflammation in a Model of Depression Induced by Chronic Stress.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Article
- Complementary and alternative medicine on cognitive defects and neuroinflammation after sepsis.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- Virtual Screening of Soybean Protein Isolate-Binding Phytochemicals and Interaction Characterization.Foods (Basel, Switzerland) · 2023Article
- The comparison of sex differences in depression-like behaviors and neuroinflammatory changes in a rat model of depression induced by chronic stress.Frontiers in behavioral neuroscience · 2022Article
- Beneficial effects of natural flavonoids on neuroinflammation.Frontiers in immunology · 2022Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicroglia activation-induced neuroinflammation may contribute to the etiology of depression.
methodsAdult Kunming mice were intraperitoneally injected vehicle or isoginkgetin (4 mg/kg) daily for 14 days before saline or LPS (0.83 mg/kg) administration. Depression-like behavior, neurotransmitter levels, and markers of neuroinflammation were determined. Isoginkgetin effect on LPS-induced microglial activation was then assessed in BV2 cells. Finally, conditioned medium (CM) derived from isoginkgetin-treated BV2 cells was co-cultured with SH-SY5Y cells for 24 h. Cell viability and apoptosis were evaluated.
resultsLPS significantly induced helplessness and anxiety, which were associated with decreased 5-HT, noradrenaline, and dopamine concentrations. Meanwhile, LPS increased microglia M1 hallmark Iba1 expression and serum interleukin (IL)-1β concentration. These changes were attenuated by isoginkgetin treatment. In vitro, isoginkgetin markedly suppressed the production of IL-1β, IL-6, tumor necrosis factor-alpha, cyclooxygenase-2, inducible nitric oxide, and reactive oxygen species, which are released from LPS-stimulated BV2 cells. More interestingly, CM from isoginkgetin-treated BV2 cells significantly alleviated SH-SY5Y cell apoptosis and restored cell viability compared to LPS-treated group through the inhibition of p38/NF-κB signaling pathway.
conclusionThese data demonstrate that isoginkgetin is an effective therapeutic agent for depression-like behaviors and neuropathological changes via potent anti-inflammatory property.
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