What question did this study set out to answer?

This research aimed to explore the effects of Obacunone on spinal cord injury, focusing on its anti-inflammatory properties and neuroprotective mechanisms.

March 14, 2026Drug Design Development and Therapy1 citationsOpen Access

Obacunone Promotes Functional Recovery After Spinal Cord Injury by Attenuating Neuroinflammation by Targeting the TLR4/MyD88/p38 MAPK Pathway

WKWenhao Kuang MZMi Zhang JZJiaqi Zhang

Key Points

This research aimed to explore the effects of Obacunone on spinal cord injury, focusing on its anti-inflammatory properties and neuroprotective mechanisms.
Utilized network pharmacology and bioinformatics for function prediction.
Conducted mouse spinal cord injury model for in vivo validation.
Assessed motor function recovery using various performance tests.
Examined spinal cord morphology using histological staining techniques.
Investigated inflammatory mechanisms using BV-2 microglial cells and a co-culture system.
Obacunone treatment significantly improved motor function in the mouse model.
Reduced inflammation and apoptosis were observed in the spinal cord.
In BV-2 cells, Oba decreased levels of pro-inflammatory cytokines after LPS exposure.
Oba showed neuroprotective effects against inflammatory apoptosis in neuron cultures.
Mechanistically, Oba inhibited the TLR4/MyD88/p38 MAPK pathway.

Abstract

Purpose: Spinal cord injury (SCI) triggers a complex secondary injury process, among which inflammation and apoptosis are the key factors of nerve injury. Obacunone (Oba) is a natural limonoid that has demonstrated a variety of pharmacological effects, but its role in SCI remains unclear. Methods: Network pharmacology and bioinformatics analysis were employed to predict the functions and mechanisms of Oba in SCI. Subsequently, in vivo validation was conducted in a mouse SCI model, with motor function recovery assessed using open field, footprint, and swimming tests. Spinal cord histomorphology was examined via hematoxylin and eosin (HE) staining and Nissl staining, while the anti‑inflammatory and anti‑apoptotic effects were evaluated by Western blot and immunofluorescence. To further elucidate the underlying mechanisms, a lipopolysaccharide (LPS)-induced inflammatory model in BV‑2 microglial cells was established to study the anti‑inflammatory mechanisms of Oba. Furthermore, a BV‑2/HT22 neuronal co‑culture system was constructed to investigate neuroprotective effects of Oba against apoptosis. Results: In vivo, Oba treatment improved motor function, promoted neural repair, reduced inflammation and apoptosis. Correspondingly, Oba suppressed the expression of LPS-induced pro-inflammatory cytokines in BV-2 cells. In a microglia-neuron co-culture system, Oba protected HT22 neurons from microglia-mediated inflammatory apoptosis. Mechanistically, the anti‑inflammatory effects of Oba were mediated by inhibiting the activation of the TLR4/MyD88/p38 MAPK pathway. Conclusion: This study identifies Oba as an effective compound that mitigates secondary injury by reducing inflammation and apoptosis and promotes nerve repair and functional recovery post-SCI, supporting its potential for further therapeutic development. Keywords: obacunone, inflammation, apoptosis, TLR4/MyD88/p38 MAPK, spinal cord injury

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Cite This Study

Kuang et al. (Sun,) studied this question.

synapsesocial.com/papers/69b4fb9db39f7826a300bf2a https://doi.org/https://doi.org/10.2147/dddt.s577707

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