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NDGA reduces secondary damage after spinal cord injury in rats via anti-inflammatory effects

机译:NDGA通过抗炎作用减少大鼠脊髓损伤后的继发性损伤

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摘要

After spinal cord injury (SCI), a series of complex pathophysiological processes follows the initial injury. Because inflammation plays a key role in this secondary pathology damage, anti-inflammatory drug treatment may reduce secondary damage and protect neurons after SCI. Though nordihydroguaiaretic acid (NDGA) can inhibit inflammatory responses, its potential roles in neuroprotection and anti- inflammation in an SCI model have not been studied. In this study, we investigated the anti-inflammatory effects of NDGA in SCI. First, histopathological alterations were evaluated with hematoxylin/eosin (HE) and Nissl staining, showing an increased number of neurons after NDGA administration. Additionally, the extent of secondary damage was assessed by TUNEL assay and measurement of astrocyte proliferation. The data showed that the numbers of apoptotic cells and the proliferative extent of astrocytes were significantly decreased by the use of NDGA. The anti-inflammatory effect of NDGA was evaluated by measuring myeloperoxidase (MPO) levels as an indicator of neutrophil activity, macrophage/microglia numbers, and expression of inflammatory cytokines including IL-1β and TNF-α. NDGA treatment significantly decreased the MPO level and the number of macrophages/microglia. In addition, NDGA also suppressed the expression of IL-1β and TNF-α after SCI. These data suggest that anti-inflammatory action by NDGA can reduce secondary damage after SCI
机译:脊髓损伤(SCI)后,最初的损伤遵循一系列复杂的病理生理过程。由于炎症在这种继发性病理损伤中起关键作用,因此抗炎药物治疗可以减少继发性损伤并保护SCI后的神经元。尽管去甲二氢愈创木酸(NDGA)可以抑制炎症反应,但尚未在SCI模型中研究其在神经保护和抗炎症中的潜在作用。在这项研究中,我们调查了NDGA在SCI中的抗炎作用。首先,用苏木精/曙红(HE)和尼氏染色评估组织病理学改变,显示NDGA给药后神经元数量增加。另外,通过TUNEL测定和星形胶质细胞增殖的测量来评估继发性损伤的程度。数据显示,通过使用NDGA,凋亡细胞的数目和星形胶质细胞的增殖程度显着降低。通过测量髓过氧化物酶(MPO)水平作为中性粒细胞活性,巨噬细胞/小胶质细胞数量以及包括IL-1β和TNF-α在内的炎性细胞因子表达的指标,来评估NDGA的抗炎作用。 NDGA处理可显着降低MPO水平和巨噬细胞/小胶质细胞数量。此外,NDGA还抑制SCI后IL-1β和TNF-α的表达。这些数据表明,NDGA的抗炎作用可以减少SCI后的继发性损害

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