Du Qixue, Meng Wei, Athari Seyyed Shamsadin, Wang Renzhong
Shandong University of Traditional Chinese Medicine, Jinan, 250001, Shandong, China.
Department of Otolaryngology, Jinan Municipal Hospital of Traditional Chinese Medicine, Jinan, 250001, Shandong, China.
Allergy Asthma Clin Immunol. 2021 Mar 20;17(1):32. doi: 10.1186/s13223-021-00534-5.
Allergic asthma is an inflammatory disease resulting from continued or intermittent allergen exposure, and allergic rhinitis can be trigger of asthma. The main mechanism of these disease is allergic reaction and immune response dysregulation. Co-Q10 is an enzyme cofactor in mitochondria can control asthma and allergic rhinitis symptoms. In the present study, we determined that the CoQ10-induced anti-allergic effects were mediated by up-regulation of Nrf2.
Animal models of allergic rhinitis and allergic asthma were produced and treated with Co-Q10, Co-Q10 and O-3, Co-Q10 and Mg-S. Bronchoalveolar lavage fluid was collected from animal models, and IL-4, 5, 13, INF-y, Eicosanoids, IgE, EPO, and histamine production were measured. Also, COX-2, CCL24, CCL11, Nrf2, Eotaxin, Cytb, COX1 and ND1 genes expressions and histopathology were studied. BALf's cells were collected by tracheostomy and used in slide producing by cytospine. Cytokines, Eicosanoids, IgE, EPO, and histamine were measured by ELISA method. Gene expression was done by Real-time PCR.
Co-Q10 with two supplementation (Mg-S and O-3) modulate MRC, BALf eosinophils, eosinophilic inflammation related genes (eotaxin, CCL11 and CCL24), peribronchial and perivascular inflammation, EPO, type 2 cytokines (IL-4, 5 and 13), IgE, histamine, Cyc-LT and LTB4 as main allergic bio-factors. Importantly, Co-Q10 treatment increased Nrf2 expression and Nrf2 induced antioxidant genes, glutathione redox and inhibited inflammation, oxidative stress injury, Th2 cytokines production and attenuated allergic inflammatory responses.
Nrf2 is activated in response to allergen, induces resistance against the rhinitis and asthma development and plays an essential role in broncho-protection. Co-Q10 increases the Nrf2 expression and the Nrf2 over-expression has strong effect in control of type2 cytokines, allergic mediators and inflammatory factors that lead to harnessing of allergy and asthma.
过敏性哮喘是一种因持续或间歇性接触过敏原而引发的炎症性疾病，过敏性鼻炎可能是哮喘的触发因素。这些疾病的主要机制是过敏反应和免疫反应失调。辅酶Q10是线粒体中的一种酶辅因子，可控制哮喘和过敏性鼻炎症状。在本研究中，我们确定辅酶Q10诱导的抗过敏作用是由Nrf2的上调介导的。
制备过敏性鼻炎和过敏性哮喘动物模型，并用辅酶Q10、辅酶Q10与O-3、辅酶Q10与Mg-S进行治疗。从动物模型中收集支气管肺泡灌洗液，检测白细胞介素-4、5、13、干扰素-γ、类二十烷酸、免疫球蛋白E、促红细胞生成素和组胺的产生。此外，研究了环氧化酶-2、趋化因子配体24、趋化因子配体11、Nrf2、嗜酸性粒细胞趋化因子、细胞色素b、环氧化酶1和NADH脱氢酶1基因的表达及组织病理学。通过气管切开术收集支气管肺泡灌洗液细胞，用于细胞离心涂片制作玻片。采用酶联免疫吸附测定法检测细胞因子、类二十烷酸、免疫球蛋白E、促红细胞生成素和组胺。通过实时聚合酶链反应进行基因表达检测。
辅酶Q10与两种补充剂（Mg-S和O-3）可调节支气管肺泡灌洗嗜酸性粒细胞、与嗜酸性粒细胞炎症相关的基因（嗜酸性粒细胞趋化因子、趋化因子配体11和趋化因子配体24）、支气管周围和血管周围炎症、促红细胞生成素、2型细胞因子（白细胞介素-4、5和13）、免疫球蛋白E、组胺、白三烯C4和白三烯B4等主要过敏生物因子。重要的是，辅酶Q10治疗可增加Nrf2表达，Nrf2诱导抗氧化基因、谷胱甘肽氧化还原，并抑制炎症、氧化应激损伤、Th2细胞因子产生，减轻过敏性炎症反应。
Nrf2在接触过敏原时被激活，诱导对鼻炎和哮喘发展的抵抗力，并在支气管保护中起重要作用。辅酶Q10可增加Nrf2表达，Nrf2的过表达对控制导致过敏和哮喘的2型细胞因子、过敏介质和炎症因子具有强大作用。
