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首页> 外文期刊>Brain research >Hydroxy-safflor yellow A attenuates A beta_(1-42)-induced inflammation by modulating the JAK2/STAT3/NF-kB pathway
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Hydroxy-safflor yellow A attenuates A beta_(1-42)-induced inflammation by modulating the JAK2/STAT3/NF-kB pathway

机译：羟基红花黄色素A通过调节JAK2 / STAT3 / NF-kB途径减轻Aβ_（1-42）诱导的炎症

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摘要

Beta-amyloid (Ap)-mediated inflammation plays a critical role in the initiation and progression of Alzheimer's disease (AD). Anti-inflammatory treatment may provide therapeutic benefits. In this study, the effect of hydroxy-safflor yellow A (HSYA) on A(3i_42-induced inflammation in AD mice was investigated and the underlying mechanisms were explored. APi_42 was injected into bilateral hippocampi of mice to induce AD models in vivo. Spatial learning and memory of mice were investigated by the Morris water maze test. Activated microglia and astrocytes were examined by immunofluorescence staining for ionized calcium-binding adapter molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP). The mRNA of inflammatory cytokines were measured using real-time PCR. NF-kB p65 translocation was analyzed by western blotting and immunostaining. kB and phosphorylation of JAK2 and STAT3 were tested by western blotting. The results showed that HSYA ameliorated the memory deficits in Ap!_^2-induced AD mice. HSYA suppressed APi^-induced activation of microglia and astrocytes and reduced the mRNA expression of pro-inflammatory mediators. HSYA up-regulated the JAK2/STAT3 pathway and inhibits the activation of NF-kB signaling pathways. Pharmacological inhibition of STAT3 by AG490 reversed the inactivation of p65 and anti-inflammatory effects of HSYA. In conclusion, these results suggest that HSYA protects Ap^-induced AD model through inhibiting inflammatory response, which may involve the JAK2/STAT3/NF-kB pathway.
机译：β淀粉样蛋白（Ap）介导的炎症在阿尔茨海默氏病（AD）的发生和发展中起关键作用。抗炎治疗可能会提供治疗益处。本研究研究了羟基番红花黄A（HSYA）对A（3i_42）引起的AD小鼠炎症的影响，并探讨了其潜在机制，将APi_42注入小鼠双侧海马体内诱导AD模型。通过莫里斯水迷宫试验研究小鼠的学习和记忆，并通过免疫荧光染色检测活化的小胶质细胞和星形胶质细胞的离子钙结合衔接分子-1（Iba-1）和胶质纤维酸性蛋白（GFAP）。实时荧光定量PCR检测细胞因子，Western blotting和免疫染色法分析NF-kB p65的易位，Western blotting检测kB以及JAK2和STAT3的磷酸化，结果表明HSYA减轻了Ap！_ ^ 2的记忆缺陷。 HSYA抑制APi ^诱导的小胶质细胞和星形胶质细胞活化，并降低促炎性介质的mRNA表达; HSYA上调JAK2 / STAT3途径和体内抑制NF-kB信号通路的激活。 AG490对STAT3的药理抑制作用可逆转p65的失活和HSYA的抗炎作用。总之，这些结果表明，HSYA通过抑制炎性反应来保护Ap 1诱导的AD模型，这可能涉及JAK2 / STAT3 / NF-kB途径。

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