Chen Hailong, Zheng Jiuqin, Ma Junjie
Department of Spinal Surgery, Luoyang Orthopedic Hospital of Henan Province (Orthopedic Hospital of Henan Province), Luoyang, Henan, China.
Department of Central Sterile Supply, Luoyang Orthopedic Hospital of Henan Province (Orthopedic Hospital of Henan Province), Luoyang, Henan, China.
Restor Neurol Neurosci. 2019;37(1):21-29. doi: 10.3233/RNN-180879.
In the search for treating neurological dysfunctions after spinal cord injury (SCI), methods of neuroprotection are of interest to intervene with the caspase pathway.
To evaluate the neuroprotective effects of vanillin in a rat model of spinal cord injury (SCI).
Rats were randomly assigned to one of three groups: a sham-operated group, and two groups where SCI was produced by ischemia/reperfusion which received either saline or vanillin (286 mg/kg, intraperitoneal [i.p.] 30 min prior to surgery). Neurological function was estimated by the Tarlov scale at 1, 12, and 24 h after surgery. Additionally, we estimated the levels of oxidative stress, inflammatory cytokines, and mitochondrial proteins in the homogenates of spinal tissues and terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) and immunohistochemical assays of spinal tissues.
Motor dysfunction was found to be significantly improved in the vanillin treated group compared to SCI rats. This was accompanied by altered levels of oxidative stress, inflammatory cytokines, and expressions of mitochondrial proteins in the SCI rats which were ameliorated by the vanillin treatment. Vanillin also significantly reduced the number of TUNEL-positive cells in spinal cord tissues compared to the sham group (p < 0.01) and decreased the number of hypoxia-inducible factor (HIF)-1α-positive cells.
In the SCI rat model vanillin exerted neuroprotective effects of reducing apoptosis and attenuating the expression of HIF-1α in spinal tissues.
在寻找治疗脊髓损伤(SCI)后神经功能障碍的方法时,神经保护方法因可干预半胱天冬酶途径而备受关注。
评估香草醛在大鼠脊髓损伤(SCI)模型中的神经保护作用。
将大鼠随机分为三组:假手术组,以及两组通过缺血/再灌注造成脊髓损伤的组,其中一组接受生理盐水,另一组接受香草醛(286毫克/千克,在手术前30分钟腹腔注射)。在手术后1、12和24小时通过塔尔洛夫量表评估神经功能。此外,我们还估计了脊髓组织匀浆中的氧化应激水平、炎性细胞因子和线粒体蛋白水平,以及脊髓组织的末端脱氧核苷酸转移酶(TdT)介导的dUTP缺口末端标记(TUNEL)和免疫组织化学分析结果。
与脊髓损伤大鼠相比,香草醛治疗组的运动功能障碍得到显著改善。这伴随着脊髓损伤大鼠氧化应激水平、炎性细胞因子的改变以及线粒体蛋白表达的变化,而香草醛治疗改善了这些变化。与假手术组相比,香草醛还显著减少了脊髓组织中TUNEL阳性细胞的数量(p < 0.01),并减少了缺氧诱导因子(HIF)-1α阳性细胞的数量。
在脊髓损伤大鼠模型中,香草醛发挥了神经保护作用,减少了脊髓组织中的细胞凋亡并减弱了HIF-1α的表达。