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Background   Spinal cord injuries (SCIs) induce secondary neuroinflammation through astrocyte reactivation, which adversely affects neuronal survival and eventually causes long-term disability. CDGSH iron sulfur domain 2 (CISD2), which has been reported to be involved in mediating the anti-inflammatory responses, can serve as a target in SCI therapy. Wild bitter melon (WBM;  Momordica charantia  Linn. var. abbreviata Ser.) contains an anti-inflammatory agent called alpha-eleostearic acid ( α -ESA), a peroxisome proliferator-activated receptor- β  (PPAR- β ) ligand. Activated PPAR- β  inhibits the nuclear factor  κ B (NF- κ B) signaling pathway via the inhibition of I κ B (inhibitor of NF- κ B) degradation. The role of astrocyte deactivation and CISD2 in anti-inflammatory mechanisms of WBM in acute SCIs is unknown.Materials and Methods   A mouse model of SCI was generated via spinal cord hemisection. The SCI mice were administered WBM intraperitoneally (500 mg/kg bodyweight). Lipopolysaccharide- (LPS-) stimulated ALT cells (astrocytes) were used as an  in vitro  model for studying astrocyte-mediated inflammation post-SCI. The roles of CISD2 and PPAR- β  in inflammatory signaling were examined using LPS-stimulated SH-SY5Y cells transfected with si-CISD2 or scramble RNA.Results   WBM mitigated the SCI-induced downregulation of CISD2, PPAR- β , and I κ B and upregulation of glial fibrillary acidic protein (GFAP; marker of astrocyte reactivation) in the spinal cord of SCI mice. Additionally, WBM (1  μ g/mL) mitigated LPS-induced CISD2 downregulation. Furthermore, SH-SY5Y neural cells with CISD2 knockdown exhibited decreased PPAR- β  expression and augmented NF- κ B signaling.Conclusion   To the best of our knowledge, this is the first study to report that CISD2 is an upstream modulator of the PPAR- β /NF- κ B proinflammatory signaling pathway in neural cells, and that WBM can mitigate the injury-induced downregulation of CISD2 in SCI mice and LPS-stimulated ALT astrocytes.

Wild Bitter Melon Exerts Anti-Inflammatory Effects by Upregulating Injury-Attenuated CISD2 Expression following Spinal Cord Injury