甘草黄酮抑制脂多糖诱导的小胶质细胞诱导型一氧化氮合酶表达
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摘要
目的探究甘草黄酮(Gla)对脂多糖(LPS)诱导的BV-2小胶质细胞一氧化碳(NO)生成和诱导型一氧化氮合酶(i NOS)表达影响。方法将BV-2细胞分为对照组、LPS组和Gla处理组,并进行相应处理。采用NO试剂盒检测NO释放量;转录聚合酶链反应(RT-PCR)法检测i NOS m RNA表达量;免疫荧光染色显示i NOS蛋白在BV-2细胞表达情况。结果 LPS刺激可显著增加BV-2小胶质细胞NO释放量和i NOS mRNA生成量(P<0.01),造成大量i-NOS阳性细胞出现,细胞体积增大,突起变粗短。Gla处理则可显著降低BV-2细胞NO释放量和i NOS mRNA生成量(P<0.01),同时i NOS阳性细胞数明显减少,细胞体积缩小,突起变细长。结论 Gla可调节BV-2细胞i-NOS表达,抑制LPS诱导的小胶质细胞神经炎症。
Objective To investigate the effects of glabridin(Gla) on NO production and i NOS expression in BV-2 microglial cells. Methods BV-2 cells were divided into the control group, LPS group and Gla treatment group and processed accordingly. The NO release was detected by NO kit, the expression of i NOS mRNA by RT-PCR, and the expression of i NOS protein by immunofluorescence staining. Results LPS stimulation significantly increased NO release and i NOS mRNA production in BV-2 microglial cells(P<0.01), resulting in a large number of i NOS-positive cells, larger cell size, thicker and shorter cell protrusions. Gla treatment significantly reduced NO release and i NOS mRNA production in BV-2 cells(P<0.01), significantly fewer i NOS-positive cells, smaller cell size, and slim cell protrusions. Conclusion Gla may regulate the i NOS expression in BV-2 cells and inhibit the neuroinflammation induced by LPS in microglial cells
Objective To investigate the effects of glabridin(Gla) on NO production and i NOS expression in BV-2 microglial cells. Methods BV-2 cells were divided into the control group, LPS group and Gla treatment group and processed accordingly. The NO release was detected by NO kit, the expression of i NOS mRNA by RT-PCR, and the expression of i NOS protein by immunofluorescence staining. Results LPS stimulation significantly increased NO release and i NOS mRNA production in BV-2 microglial cells(P<0.01), resulting in a large number of i NOS-positive cells, larger cell size, thicker and shorter cell protrusions. Gla treatment significantly reduced NO release and i NOS mRNA production in BV-2 cells(P<0.01), significantly fewer i NOS-positive cells, smaller cell size, and slim cell protrusions. Conclusion Gla may regulate the i NOS expression in BV-2 cells and inhibit the neuroinflammation induced by LPS in microglial cells
引文
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[2] Ramirez AI, de Hoz R, Salobrar-Garcia E, et al. The role of microglia in retinal neurodegeneration:Alzheimer′s disease,Parkinson, and glaucoma[J]. Front Aging Neurosci,2017,6(9):214.
[3] Tan W, Cao XB, Tian Z, et al. Effects of simvastatin on the expression of inducible nitric oxide synthase and brain-derived neurotrophic factor in a lipopolysaccharide-induced rat model of Parkinson disease[J]. Int J Neurosci,2016,126(3):278-286.
[4] Cárdenas A, Moro MA, Hurtado O, et al. Dual role of nitric oxide in adult neurogenesis[J]. Brain Res Rev,2005,50(1):1-6.
[5]陈浩,师亮,王燕宏,等.甘草黄酮对MPTP帕金森病小鼠的实验性治疗研究[J].中风与神经疾病杂志,2013,30(12):1112-1113.
[6]赵焱,卢祖能.光甘草定对MPTP致帕金森病小鼠海马区ERK信号通路的影响[J].中华医学杂志,2017,97(26):2050-2054.
[7]肖辉.甘草黄酮对UVB诱导Ha CaT细胞ERS中IRE1信号通路的影响[D].兰州:兰州大学,2016.
[8] Ling Z, Zhu Y, Cw T, et al. Progressive dopamine neuron loss following supra-nigral lipopolysaccharide(LPS)infusion into rats exposed to LPS prenatally[J]. Exp Neurol. 2006,199(2):499-512.
[9] Arimoto T, Bing G. Up-regulation of inducible nitric oxide synthase in the substantia nigra by lipopolysaccharide causes microglial activation and neurodegeneration[J]. Neurobiol Dis,2003,12(1):35-45.
[10]姜牧君,陈育华,屈晓龙,等. LPS诱导慢性帕金森病小鼠模型的建立与评价[J].解剖学研究,2016,38(5):391-395,426.
[11] Kang MR, Park KH, Oh SJ, et al. Cardiovascular protective effect of glabridin:Implications in LDL oxidation and inflammation[J]. Int Immunopharmacol,2015,29(2):914-918.
[12] Xie YC, Dong XW,Wu XM,et al. Inhibitory effects of flavonoids extracted from licorice on lipopolysaccharide-induced acute pulmonary inflammation in mice[J]. Int Immunopharmacol,2009,9(2):194-200.
[13] Thiyagarajan P, Chandrasekaran CV, Deepak HB, et al. Modulation of lipopolysaccharide-induced pro-inflammatory mediators by an extract of Glycyrrhiza glabra and its phytoconstituents[J].Inflammopharmacology,2011,19(4):235-241.