ArticleBMC complementary medicine and therapies2025
Cibotii Rhizoma extract protects rat dorsal root ganglion neurons against H
Article in BMC complementary medicine and therapies, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundDorsal root ganglion (DRG) neurons are particularly susceptible to oxidative injury, which contributes to neuronal apoptosis and altered pain signaling. Oxidative stress in DRG neurons plays a pivotal role in the onset and maintenance of pain hypersensitivity under pathological conditions. We aimed to investigate the neuroprotective effects of Cibotii Rhizoma (CR) in rat DRG neurons subjected to H₂O₂-induced oxidative stress.
methodsPrimary DRG neurons were isolated from 5-week-old Sprague–Dawley rats and cultured under short-term and long-term protocols. Cells were treated with CR (10–400 µg/mL) and exposed to H₂O₂. Cell viability was assessed by Cell Counting Kit-8 assay, and antioxidant effects were evaluated via DCFDA and MitoSOX-based flow cytometry and immunocytochemistry. Neurite outgrowth was analyzed using Tuj1 staining, and pain-related markers (CGRP, IB4, TRPV1, and substance P) were examined in long-term cultures. Molecular docking was performed to assess TRPV1 binding affinity of CR-derived compounds.
resultsCR showed no cytotoxicity up to 400 µg/mL and significantly protected DRG neurons from 10 µg/mL against H2O2-induced oxidative stress. CR promoted neurite outgrowth and reduced oxidative stress markers (DCFDA⁺ and MitoSOX⁺ cells) within the 10–50 µg/mL concentration range, dose-dependently. Pain-related proteins (CGRP, IB4, TRPV1) and substance P were upregulated by H₂O₂ but significantly decreased following CR treatment. Molecular docking identified several CR-derived compounds with high binding affinity to TRPV1 may attenuate pain signaling pathways.
conclusionsCR confers neuroprotection against oxidative stress in DRG neurons and modulates pain-related signaling pathways, highlighting its potential as a therapeutic agent for oxidative stress-induced neuropathic pain.
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