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本文引用的文献

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Study on the inflammatory intervention of erythropoietin on NEC.促红细胞生成素对坏死性小肠结肠炎的炎症干预研究。
Exp Ther Med. 2016 Jun;11(6):2221-2224. doi: 10.3892/etm.2016.3199. Epub 2016 Mar 29.
2
Effect of salvianolic acid A and C compatibility on inflammatory cytokines in rats with unilateral ureteral obstruction.丹酚酸A与C配伍对单侧输尿管梗阻大鼠炎性细胞因子的影响
J Tradit Chin Med. 2015 Oct;35(5):564-70. doi: 10.1016/s0254-6272(15)30140-0.
3
Bloodstream infections during the onset of necrotizing enterocolitis and their relation with the pro-inflammatory response, gut wall integrity and severity of disease in NEC.坏死性小肠结肠炎发病期间的血流感染及其与坏死性小肠结肠炎中促炎反应、肠壁完整性和疾病严重程度的关系。
J Pediatr Surg. 2015 Nov;50(11):1837-41. doi: 10.1016/j.jpedsurg.2015.07.009. Epub 2015 Jul 14.
4
Astragaloside IV attenuates injury caused by myocardial ischemia/reperfusion in rats via regulation of toll-like receptor 4/nuclear factor-κB signaling pathway.黄芪甲苷通过调节 Toll 样受体 4/核因子-κB 信号通路减轻大鼠心肌缺血再灌注损伤。
Phytother Res. 2015 Apr;29(4):599-606. doi: 10.1002/ptr.5297. Epub 2015 Jan 21.
5
Antiasthmatic Effects of Eugenol in a Mouse Model of Allergic Asthma by Regulation of Vitamin D3 Upregulated Protein 1/NF-κB Pathway.丁香酚通过调节维生素D3上调蛋白1/核因子κB通路对过敏性哮喘小鼠模型的抗哮喘作用
Inflammation. 2015 Aug;38(4):1385-93. doi: 10.1007/s10753-015-0110-8.
6
Intestinal epithelial MyD88 is a sensor switching host metabolism towards obesity according to nutritional status.肠道上皮细胞中的髓样分化因子88(MyD88)是一种传感器,可根据营养状况将宿主代谢转换为有利于肥胖的状态。
Nat Commun. 2014 Dec 5;5:5648. doi: 10.1038/ncomms6648.
7
Pathogenesis of necrotizing enterocolitis: modeling the innate immune response.坏死性小肠结肠炎的发病机制:模拟先天免疫反应
Am J Pathol. 2015 Jan;185(1):4-16. doi: 10.1016/j.ajpath.2014.08.028. Epub 2014 Nov 4.
8
Astragaloside IV inhibits platelet-derived growth factor-BB-stimulated proliferation and migration of vascular smooth muscle cells via the inhibition of p38 MAPK signaling.黄芪甲苷IV通过抑制p38丝裂原活化蛋白激酶信号通路,抑制血小板衍生生长因子-BB刺激的血管平滑肌细胞增殖和迁移。
Exp Ther Med. 2014 Oct;8(4):1253-1258. doi: 10.3892/etm.2014.1905. Epub 2014 Aug 14.
9
Rice prolamin extract ameliorates acute murine colitis by inhibiting nuclear factor-kappa B and modulating intestinal apoptosis and cell proliferation.大米醇溶蛋白提取物通过抑制核因子-κB和调节肠道细胞凋亡及细胞增殖来改善急性小鼠结肠炎。
Clin Exp Immunol. 2014 Dec;178(3):537-47. doi: 10.1111/cei.12431.
10
Astragaloside IV attenuates experimental autoimmune encephalomyelitis of mice by counteracting oxidative stress at multiple levels.黄芪甲苷通过多水平对抗氧化应激来减轻实验性自身免疫性脑脊髓炎的小鼠模型。
PLoS One. 2013 Oct 4;8(10):e76495. doi: 10.1371/journal.pone.0076495. eCollection 2013.

黄芪甲苷IV通过维生素D3上调蛋白1/核因子κB信号通路减轻氧化应激和抑制炎症来改善坏死性小肠结肠炎。

Astragaloside IV ameliorates necrotizing enterocolitis by attenuating oxidative stress and suppressing inflammation via the vitamin D3-upregulated protein 1/NF-κB signaling pathway.

作者信息

Cai Zhiyong, Liu Jindi, Bian Hongliang, Cai Jinlan

机构信息

Newborn Department, Yancheng Maternity and Child Health Care Hospital, Yancheng, Jiangsu 224000, P.R. China.

出版信息

Exp Ther Med. 2016 Oct;12(4):2702-2708. doi: 10.3892/etm.2016.3629. Epub 2016 Aug 30.

DOI:10.3892/etm.2016.3629
PMID:27698775
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5038370/
Abstract

Astragaloside IV (AS-IV) is a flavonoid from the plant (Fisch) Bge that has a wide range of therapeutic effects. The aim of the present study was to examine the effect of AS-IV on rats with necrotizing enterocolitis (NEC) under oxidative stress and inflammation. Newborn Sprague-Dawley rats were induced with NEC by asphyxia and hypothermia applied on 3 consecutive days. The rats were orally administered AS-IV at 25, 50 and 75 mg/kg for 4 days. The results revealed that AS-IV administration prevented NEC-induced decrease in the concentration of malondialdehyde and myeloperoxidase, and increase in the activity of glutathione (GSH) and superoxide dismutase in murine models. AS-IV also inhibited NEC-induced elevation in the levels of interleukin (IL)-6, IL-1β, tumor necrosis factor-α and nuclear factor (NF)-κB. The effects of AS-IV were achieved under inflammation and oxidative stress. Western blotting demonstrated that AS-IV substantially inhibited the phosphorylated (p)-IκBα, NF-κBp65, p-NF-κBp65 protein levels and increased vitamin D3 upregulated protein 1 (VDUP1) and IκBα protein levels. These data indicate that AS-IV may be effective in the protection of NEC-induced ileum degeneration by inhibiting the levels of inflammatory markers and oxidative stress via the regulation of the VDUP1/NF-κB signaling pathway.

摘要

黄芪甲苷IV(AS-IV)是一种从植物蒙古黄芪(Fisch)Bge中提取的黄酮类化合物,具有广泛的治疗作用。本研究的目的是研究AS-IV在氧化应激和炎症条件下对坏死性小肠结肠炎(NEC)大鼠的影响。通过连续3天施加窒息和低温诱导新生Sprague-Dawley大鼠发生NEC。将大鼠分别以25、50和75 mg/kg的剂量口服给予AS-IV,持续4天。结果显示,在小鼠模型中,给予AS-IV可防止NEC诱导的丙二醛和髓过氧化物酶浓度降低,以及谷胱甘肽(GSH)和超氧化物歧化酶活性增加。AS-IV还抑制了NEC诱导的白细胞介素(IL)-6、IL-1β、肿瘤坏死因子-α和核因子(NF)-κB水平升高。AS-IV的这些作用是在炎症和氧化应激条件下实现的。蛋白质印迹法表明,AS-IV可显著抑制磷酸化(p)-IκBα、NF-κBp65、p-NF-κBp65蛋白水平,并增加维生素D3上调蛋白1(VDUP1)和IκBα蛋白水平。这些数据表明,AS-IV可能通过调节VDUP1/NF-κB信号通路抑制炎症标志物水平和氧化应激,从而有效保护NEC诱导的回肠变性。