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

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題名:	Wild Bitter Melon Exerts Anti-Inflammatory Effects by Upregulating Injury-Attenuated CISD2 Expression following Spinal Cord Injury
作者:	Kung, WM (Kung, Woon-Man) Lin, CC (Lin, Chai-Ching) Kuo, CY (Kuo, Chan-Yen) Juin, YC (Juin, Yu-Ching) Wu, PC (Wu, Po-Ching) Lin, MS (Lin, Muh-Shi)
貢獻者:	運健系
關鍵詞:	VAR.-ABBREVIATA-SER CONJUGATED LINOLEIC-ACID ALPHA-ELEOSTEARIC ACID INFLAMMATORY RESPONSE MITOCHONDRIAL DYSFUNCTION PPAR-DELTA ASTROCYTES AUTOPHAGY CURCUMIN ANTIOXIDANT
日期:	2020-09-30
上傳時間:	2020-11-09 10:42:01 (UTC+8)
摘要:	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 charantiaLinn. var. abbreviata Ser.) contains an anti-inflammatory agent called alpha-eleostearic acid (alpha-ESA), a peroxisome proliferator-activated receptor-beta(PPAR-beta) ligand. Activated PPAR-beta inhibits the nuclear factor kappa B (NF-kappa B) signaling pathway via the inhibition of I kappa B (inhibitor of NF-kappa 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 anin vitromodel for studying astrocyte-mediated inflammation post-SCI. The roles of CISD2 and PPAR-beta 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-beta, and I kappa B and upregulation of glial fibrillary acidic protein (GFAP; marker of astrocyte reactivation) in the spinal cord of SCI mice. Additionally, WBM (1 mu g/mL) mitigated LPS-induced CISD2 downregulation. Furthermore, SH-SY5Y neural cells with CISD2 knockdown exhibited decreased PPAR-beta expression and augmented NF-kappa 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-beta/NF-kappa 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.
關聯:	BEHAVIOURAL NEUROLOGY 卷冊: 2020 文獻號碼: 1080521
顯示於類別:	[運動與健康促進學系] 期刊論文

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