Neural Regeneration Research ›› 2016, Vol. 11 ›› Issue (2): 222-223.doi: 10.4103/1673-5374.177718

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New insight into curcumin-based therapy in spinal cord injuries: CISD2 regulation

Chai-Ching Lin, Muh-Shi Lin   

  1. Department of Neurosurgery, Taipei City Hospital, Zhong Xiao Branch, Taipei, Taiwan, China (Lin MS)
    Department of Surgery, Faculty of Medicine, School of Medicine,
    National Yang-Ming University, Taipei, Taiwan, China (Lin MS)
    Department of Biotechnology and Animal Science, College of
    Bioresources, National Ilan University, Yilan, Taiwan, China (Lin CC, Lin MS)
  • Received:2015-12-25 Online:2016-02-15 Published:2016-02-15
  • Contact: Muh-Shi Lin, M.D., Ph.D., LL.M.,neurosurgery2005@yahoo.com.tw.
  • Supported by:

    This work was supported by grants from the Taipei Institute of Pathology, Taiwan (TIP10102A), the Taipei City Hospital, Taiwan (TPCH-102-061 and TPCH-104-043) and the Department of Health, Taipei City Government (10401-62-038).

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Abstract:

CDGSH iron sulfur domain 2 (CISD2) (synonyms: NAF-1, Eris, Miner1 and Noxp70) was originally regarded as a survival gene, based on its roles in calcium metabolism, anti-apoptosis, and longevity. Furthermore, CISD2 has been shown to inhibit an increase in excitotoxic Ca2+ at the endoplasmic reticulum, via a combination between BCL2 and the inositol 1,4,5-triphosphate receptor. CISD2 helps to prevent mitochondrial dysfunction and subsequent cell death. Our research team also found that CISD2 plays a moderating role in traumatic spinal cord injuries. The authors previously identified the injury-induced down-regulation of CISD2 expression in an animal model of SCI as well as in a cell culture model of astrocyte reactivation. Using primary impact and hemisection to adjust injury severity, animals subjected to SCI presented a signi?cant upregulation of proin?ammatory mediators, including inducible nitric oxide synthase (iNOS) and RANTES (Regulated on Activation, Normal T Cell Expressed and Secreted) as well as a downregulation of CISD2 mRNA and protein expression. It has been postulated that SCI causes inflammatory responses and a drop in CISD2 levels. Furthermore, CISD2 inactivity has been proposed as a mechanism underlying secondary damage following SCI. Curcumin exhibits multiple pharmacologic effects, such as anti-in?ammatory, anticarcinogenic, anti-infection, antioxidant, and hypocholesterolemic activities. The neuroprotective benefits stemming from the anti-inflammatory effects of curcumin have been demonstrated in cases of SCI. The pharmacological effects of curcumin clearly involve the regulation of CISD2. Briefly, injury to the spinal cord downregulates the expression of CISD2; however, curcumin has been shown to attenuate the downregulation of CISD2 in SCI and LPS-treated astrocytes. The ability of curcumin to prolong the expression of CISD2 could be of therapeutic value in SCI therapy. The anti-apoptosis and attenuation of NO production by CISD2 may account for the neuroprotective effects of curcumin in the treatment of SCI.