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阿魏酸对大鼠脊髓缺血再灌注损伤的神经保护作用。

The Neuroprotective Effect of Syringic Acid on Spinal Cord Ischemia/Reperfusion Injury in Rats.

机构信息

Department of Neurosurgery, Faculty of Medicine, Medipol University, Istanbul, Turkey,

出版信息

Inflammation. 2015 Oct;38(5):1969-78. doi: 10.1007/s10753-015-0177-2.

Abstract

Acute arterial occlusions via different vascular pathologies are the main causes of spinal cord ischemia. We investigated neuroprotective effects of syringic acid on spinal cord ischemia injury in rats. Rats were divided into four groups: (I) sham-operated control rats, (II) spinal cord ischemia group, (III) spinal cord ischemia group performed syringic acid, and (IV) spinal cord ischemia group performed methylprednisolone intraperitoneally. Spinal cord ischemia was performed by the infrarenal aorta cross-clamping model. The spinal cord was removed after the procedure. The biochemical and histopathological changes were observed within the samples. Functional assessment was performed for neurological deficit scores. A significant decrease was seen in malondialdehyde levels in group III as compared to group II (P < 0.05). Besides these, nuclear respiratory factor-1 and superoxide dismutase activity of group III were significantly higher than group II (P < 0.05). In histopathological samples, when group III was compared with group II, there was a significant decrease in numbers of apoptotic neurons (P < 0.05). In immunohistochemical staining, BECN1 and caspase-3-immunopositive neurons were significantly decreased in group III compared with group II (P < 0.05). The neurological deficit scores of group III were significantly higher than group II at twenty-fourth hour of ischemia (P < 0.05). Our study revealed that syringic acid pretreatment in spinal cord ischemia/reperfusion reduced oxidative stress and neuronal degeneration as a neuroprotective agent. Ultrastructural studies are required for syringic acid to be developed as a promising therapeutic agent to be utilized for human spinal cord ischemia in the future.

摘要

不同血管病变导致的急性动脉闭塞是脊髓缺血的主要原因。我们研究了原儿茶酸对大鼠脊髓缺血损伤的神经保护作用。大鼠分为四组:(I)假手术对照组,(II)脊髓缺血组,(III)脊髓缺血组给予原儿茶酸,(IV)脊髓缺血组给予甲基强的松龙腹腔内注射。通过肾下腹主动脉夹闭模型进行脊髓缺血。手术后取出脊髓。观察样本中的生化和组织病理学变化。进行神经功能缺损评分进行功能评估。与 II 组相比,III 组丙二醛水平显著降低(P<0.05)。除此之外,III 组核呼吸因子-1 和超氧化物歧化酶活性明显高于 II 组(P<0.05)。在组织病理学样本中,与 II 组相比,III 组凋亡神经元数量明显减少(P<0.05)。在免疫组织化学染色中,与 II 组相比,III 组 BECN1 和 caspase-3 免疫阳性神经元明显减少(P<0.05)。缺血 24 小时时,III 组的神经功能缺损评分明显高于 II 组(P<0.05)。我们的研究表明,原儿茶酸预处理可减轻脊髓缺血/再灌注后的氧化应激和神经元变性,作为一种神经保护剂。需要进行超微结构研究,以将原儿茶酸开发为一种有前途的治疗剂,用于未来人类脊髓缺血。

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