The pathogenesis of cervical spondylotic myelopathy (CSM) is related to both primary mechanical and secondary biological injury. The authors of this study explored a novel, noninvasive method of promoting neuroprotection in myelopathy by using curcumin to minimize oxidative cellular injury and the capacity of omega-3 fatty acids to support membrane structure and improve neurotransmission.
An animal model of CSM was created using a nonresorbable expandable polymer placed in the thoracic epidural space, which induced delayed myelopathy. Animals that underwent placement of the expandable polymer were exposed to either a diet rich in docosahexaenoic acid and curcumin (DHA-Cur) or a standard Western diet (WD). Twenty-seven animals underwent serial gait testing, and spinal cord molecular assessments were performed after the 6-week study period.
At the conclusion of the study period, gait analysis revealed significantly worse function in the WD group than in the DHA-Cur group. Levels of brain-derived neurotrophic factor (BDNF), syntaxin-3, and 4-hydroxynonenal (4-HNE) were measured in the thoracic region affected by compression and lumbar enlargement. Results showed that BDNF levels in the DHA-Cur group were not significantly different from those in the intact animals but were significantly greater than in the WD group. Significantly higher lumbar enlargement syntaxin-3 in the DHA-Cur animals combined with a reduction in lipid peroxidation (4-HNE) indicated a possible healing effect on the plasma membrane.
Data in this study demonstrated that DHA-Cur can promote spinal cord neuroprotection and neutralize the clinical and biochemical effects of myelopathy.
Abbreviations used in this paper:AdV-BDNF = adenovirusmediated BDNF; BDNF = brain-derived neurotrophic factor; CSM = cervical spondylotic myelopathy; Cur = curcumin; DHA = docosahexaenoic acid; SCI = spinal cord injury; WD = Western diet; 4-HNE = 4-hydroxynonenal.
Address correspondence to: Langston T. Holly, M.D., Department of Neurosurgery, David Geffen School of Medicine at UCLA, Center for the Health Sciences, Box 956901, Los Angeles, California 90095-6901. email: email@example.com.
Please include this information when citing this paper: published online June 26, 2012; DOI: 10.3171/2012.5.SPINE1216.
MerendaA, , GugliottaM, , HollowayR, , LevasseurJE, , AlessandriB, & SunD, : Validation of brain extracellular glycerol as an indicator of cellular membrane damage due to free radical activity after traumatic brain injury. J Neurotrauma25:527–537, 2008
MerendaA, GugliottaM, HollowayR, LevasseurJE, AlessandriB, SunD, : Validation of brain extracellular glycerol as an indicator of cellular membrane damage due to free radical activity after traumatic brain injury. J Neurotrauma25:527–537, 2008)| false
SharmaS, , ZhuangY, , YingZ, , WuA, & Gomez-PinillaF: Dietary curcumin supplementation counteracts reduction in levels of molecules involved in energy homeostasis after brain trauma. Neuroscience161:1037–1044, 2009
SharmaS, ZhuangY, YingZ, WuA, Gomez-PinillaF: Dietary curcumin supplementation counteracts reduction in levels of molecules involved in energy homeostasis after brain trauma. Neuroscience161:1037–1044, 2009)| false