Safranal Alleviated OVA-Induced Asthma Model and Inhibits Mast Cell Activation.
Safranal Alleviated OVA-Induced Asthma Model and Inhibits Mast Cell Activation.
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Safranal 减轻 OVA 诱发的哮喘模型并抑制肥大细胞激活
DOI：
10.3389/fimmu.2021.585595
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发表时间：
2021
影响因子：
7.3
通讯作者：
Xu H
中科院分区：
文献类型：
--
作者：
Lertnimitphun P;Zhang W;Fu W;Yang B;Zheng C;Yuan M;Zhou H;Zhang X;Pei W;Lu Y;Xu H
哮喘是一种慢性、反复发作的气道疾病，与肥大细胞活化有关。从中草药中提取的许多化合物具有稳定肥大细胞和减少炎症介质产生的作用。番红花醛是番红花中的一种活性成分，具有多种抗炎作用。本研究探讨了番红花醛对卵清蛋白（OVA）诱导的哮喘模型的作用。在被动全身过敏反应（PSA）模型中，研究番红花醛对肥大细胞的稳定作用及对炎症介质产生的抑制作用。方法采用卵白蛋白诱发哮喘和前列腺特异性抗原（PSA）模型，观察番红醛的体内作用。收集肺组织用于H&E、TB、IHC和PAS染色。采用ELISA法检测血清IgE水平和趋化因子IL-4、IL-5、TNF-α、IFN-γ水平。RNA测序被用来揭示番红花醛调控的基因。采用骨髓源性肥大细胞（BMMCs）研究番红醛的抑制作用及其机制。评估了细胞因子（IL-6、TNF-α和LTC 4）的产生以及NF-κB和MAPKs信号通路。结果番红花醛可降低哮喘小鼠血清IgE水平，减少肺组织肥大细胞数量，使Th 1/Th 2细胞因子水平恢复正常。此外，番红花醛还能抑制BMMCs脱颗粒，抑制LTC 4、IL-6和TNF-α的产生。番红花醛抑制NF-κB和MAPK途径蛋白磷酸化，减少NF-κB p65、AP-1核转位。在PSA模型中，番红花醛降低血清中组胺和LTC 4的水平。结论番红花醛可对抗OVA诱导的哮喘，抑制肥大细胞活化和PSA反应。其可能的机制是通过抑制MAPK和NF-κB通路。
Introduction Asthma is a chronic and recurring airway disease, which related to mast cell activation. Many compounds derived from Chinese herbal medicine has promising effects on stabilizing mast cells and decreasing inflammatory mediator production. Safranal, one of the active compounds from Crocus sativus, shows many anti-inflammatory properties. In this study, we evaluated the effect of safranal in ovalbumin (OVA)-induced asthma model. Furthermore, we investigate the effectiveness of safranal on stabilizing mast cell and inhibiting the production of inflammatory mediators in passive systemic anaphylaxis (PSA) model. Methods OVA-induced asthma and PSA model were used to evaluate the effect of safranal in vivo. Lung tissues were collected for H&E, TB, IHC, and PAS staining. ELISA were used to determine level of IgE and chemokines (IL-4, IL-5, TNF-α, and IFN-γ). RNA sequencing was used to uncovers genes that safranal regulate. Bone marrow-derived mast cells (BMMCs) were used to investigate the inhibitory effect and mechanism of safranal. Cytokine production (IL-6, TNF-α, and LTC4) and NF-κB and MAPKs signaling pathway were assessed. Results Safranal reduced the level of serum IgE, the number of mast cells in lung tissue were decreased and Th1/Th2 cytokine levels were normalized in OVA-induced asthma model. Furthermore, safranal inhibited BMMCs degranulation and inhibited the production of LTC4, IL-6, and TNF-α. Safranal inhibits NF-κB and MAPKs pathway protein phosphorylation and decreases NF-κB p65, AP-1 nuclear translocation. In the PSA model, safranal reduced the levels of histamine and LTC4 in serum. Conclusions Safranal alleviates OVA-induced asthma, inhibits mast cell activation and PSA reaction. The possible mechanism occurs through the inhibition of the MAPKs and NF-κB pathways.
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DOI：
10.1016/j.jaci.2016.01.049
发表时间：
2016-09
期刊：
The Journal of allergy and clinical immunology
影响因子：
--
作者：
Bryce PJ;Falahati R;Kenney LL;Leung J;Bebbington C;Tomasevic N;Krier RA;Hsu CL;Shultz LD;Greiner DL;Brehm MA
通讯作者：
Brehm MA
影响因子：
48
作者：
Langmead, Ben;Salzberg, Steven L.
通讯作者：
Salzberg, Steven L.
伊马替尼在严重难治性哮喘患者中抑制试剂盒。
DOI：
10.1056/nejmoa1613125
发表时间：
2017-05-18
期刊：
The New England journal of medicine
影响因子：
--
作者：
Cahill KN;Katz HR;Cui J;Lai J;Kazani S;Crosby-Thompson A;Garofalo D;Castro M;Jarjour N;DiMango E;Erzurum S;Trevor JL;Shenoy K;Chinchilli VM;Wechsler ME;Laidlaw TM;Boyce JA;Israel E
通讯作者：
Israel E
影响因子：
5.6
作者：
Park, Hee-ju;Lee, Chang-Min;Park, Yeong-Min
通讯作者：
Park, Yeong-Min
影响因子：
6.1
作者：
Kassel, O;De Blay, F;Frossard, N
通讯作者：
Frossard, N