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白藜芦醇通过抑制炎症和氧化应激反应减轻大鼠脊髓损伤。

The effects of oxyresveratrol abrogates inflammation and oxidative stress in rat model of spinal cord injury.

机构信息

Department of Orthopedics, Hebei Cangzhou Central Hospital, Cangzhou, Hebei 061000, P.R. China.

出版信息

Mol Med Rep. 2018 Mar;17(3):4067-4073. doi: 10.3892/mmr.2017.8294. Epub 2017 Dec 18.

DOI:10.3892/mmr.2017.8294
PMID:29257323
Abstract

Oxyresveratrol and its glycoside are important natural active materials. As an effective tyrosine kinase inhibitor, oxyresveratrol may prevent herpes virus infection, inflammation and oxidative stress, as well as protect nerves. In addition, it is known to inhibit cell apoptosis following cerebral ischemia. In recent years, oxyresveratrol and its glycoside have been widely investigated, and their useful biological activities have been explored, indicating that they may be worthy of further comprehensive research. The aim of the present study was to evaluate the photoprotective effects of oxyresveratrol and its ability to abrogate inflammation and oxidative stress in a rat model of spinal cord injury (SCI). The authors identified that oxyresveratrol significantly reversed the SCI‑induced inhibition of Basso, Beattie, and Bresnahan scores, inhibited the SCI‑mediated increase in spinal cord water content, significantly suppressed SCI‑induced nuclear factor‑κB/p65, tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑6 activities and reversed the malondialdehyde, superoxide dismutase, glutathione (GSH) and GSH peroxidase activities in SCI rats. SCI‑induced granulocyte‑macrophage colony‑stimulating factor (GM‑CSF), inducible nitric oxide synthase (iNOS) and cyclo‑oxygenase‑2 (COX‑2) protein expression was significantly suppressed by oxyresveratrol, and SCI‑mediated inhibition of nuclear factor (erythroid‑derived 2)‑like 2 (Nrf2) protein expression was significantly increased by oxyresveratrol. In conclusion, these results suggest that the effects of oxyresveratrol restores SCI, and abrogates inflammation and oxidative stress in rat model of SCI via the GM‑CSF, iNOS, COX‑2 and Nrf2 signaling pathway.

摘要

白藜芦醇及其糖苷是重要的天然活性物质。作为一种有效的酪氨酸激酶抑制剂,白藜芦醇可能预防疱疹病毒感染、炎症和氧化应激,保护神经。此外,它被认为可抑制脑缺血后的细胞凋亡。近年来,白藜芦醇及其糖苷已得到广泛研究,其有益的生物学活性得到了探索,表明它们可能值得进一步全面研究。本研究旨在评估白藜芦醇及其减轻炎症和氧化应激的能力对脊髓损伤(SCI)大鼠模型的光保护作用。作者发现,白藜芦醇显著逆转了 SCI 诱导的 Basso、Beattie 和 Bresnahan 评分抑制,抑制了脊髓含水量的增加,显著抑制了 SCI 介导的核因子-κB/p65、肿瘤坏死因子-α、白细胞介素(IL)-1β和 IL-6 活性,并逆转了 SCI 大鼠的丙二醛、超氧化物歧化酶、谷胱甘肽(GSH)和 GSH 过氧化物酶活性。SCI 诱导的粒细胞-巨噬细胞集落刺激因子(GM-CSF)、诱导型一氧化氮合酶(iNOS)和环氧化酶-2(COX-2)蛋白表达被白藜芦醇显著抑制,SCI 介导的核因子(红细胞衍生 2)样 2(Nrf2)蛋白表达被白藜芦醇显著增加。综上所述,这些结果表明,白藜芦醇通过 GM-CSF、iNOS、COX-2 和 Nrf2 信号通路恢复 SCI,并减轻 SCI 大鼠模型的炎症和氧化应激。

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