Department of Neurosurgery, Gazi University Faculty of Medicine, Beşevler;
J Neurosurg Spine. 2014 Apr;20(4):464-70. doi: 10.3171/2013.12.SPINE1312. Epub 2014 Jan 24.
The object of this study was to conduct a prospective, randomized, laboratory investigation of the neuroprotective effects of curcumin functionally, biochemically, and histologically in an experimental acute spinal cord ischemia-reperfusion injury on rabbits.
Eighteen rabbits were randomly assigned to 1 of 3 groups: the sham group, the ischemia-reperfusion group, or the curcumin group. Spinal cord ischemia was induced by applying an infrarenal aortic cross-clamp for 30 minutes. At 48 hours after ischemia, neurological function was evaluated with modified Tarlov criteria. Biochemical changes in the spinal cord and plasma were observed by measuring levels of malondialdehyde (MDA), advanced oxidation protein products (AOPP), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), nitrite/nitrate, and tumor necrosis factor-α (TNF-α). Histological changes were examined with H & E staining. Immunohistochemical staining with antibodies against caspase-3 was performed to evaluate cell apoptosis after ischemia.
In the curcumin group, neurological outcome scores were statistically significantly better compared with the ischemia-reperfusion group. In the ischemia-reperfusion group, MDA, AOPP, and nitrite/nitrate levels were significantly elevated in the spinal cord tissue and the plasma by the induction of ischemia-reperfusion. The curcumin treatment significantly prevented the ischemia-reperfusion-induced elevation of nitrite/nitrate and TNF-α. In addition, the spinal cord tissue and the plasma SOD, GSH, and CAT levels were found to be preserved in the curcumin group and not statistically different from those of the sham group. Histological evaluation of the tissues also demonstrated a decrease in axonal damage, neuronal degeneration, and glial cell infiltration after curcumin administration.
Although further studies including different dose regimens and time intervals are required, curcumin could attenuate a spinal cord ischemia-reperfusion injury in rabbits via reducing oxidative products and proinflammatory cytokines, as well as increasing activities of antioxidant enzymes and preventing apoptotic cell death.
本研究旨在通过实验性急性脊髓缺血再灌注损伤兔模型，从功能、生化和组织学角度对姜黄素的神经保护作用进行前瞻性、随机、实验室研究。
将 18 只兔子随机分为 3 组：假手术组、缺血再灌注组和姜黄素组。通过应用肾下主动脉夹闭 30 分钟来诱导脊髓缺血。在缺血后 48 小时，采用改良 Tarlov 标准评估神经功能。通过测量丙二醛（MDA）、晚期氧化蛋白产物（AOPP）、谷胱甘肽（GSH）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、亚硝酸盐/硝酸盐和肿瘤坏死因子-α（TNF-α）的水平来观察脊髓和血浆中的生化变化。用 H & E 染色观察组织学变化。用针对半胱氨酸天冬氨酸蛋白酶-3（caspase-3）的抗体进行免疫组织化学染色，以评估缺血后细胞凋亡情况。
与缺血再灌注组相比，姜黄素组的神经功能评分明显更好。在缺血再灌注组，通过诱导缺血再灌注，脊髓组织和血浆中的 MDA、AOPP 和亚硝酸盐/硝酸盐水平显著升高。姜黄素治疗可显著防止缺血再灌注引起的亚硝酸盐/硝酸盐和 TNF-α升高。此外，在姜黄素组中，脊髓组织和血浆中的 SOD、GSH 和 CAT 水平得到保存，与假手术组相比无统计学差异。组织学评估还表明，姜黄素给药后轴突损伤、神经元变性和神经胶质细胞浸润减少。
尽管需要进一步研究，包括不同的剂量方案和时间间隔，但姜黄素可能通过减少氧化产物和促炎细胞因子，增加抗氧化酶的活性并防止细胞凋亡，从而减轻兔脊髓缺血再灌注损伤。
