The Study On The Effect Of The Allergic Asthma Of Mice Promoted By Graphene Oxide

Nowadays, nanomaterials have been used widely in a number of applications in life. However, these nanomaterials could also result in risk to the environment and human health, particularly to the respiratory system. Graphene is one of the most application prospects of nanomaterials, and one of the most important derivatives of it is graphene oxide (GO) which is characterized by a few of surface oxygenic functional groups, including hydroxyl, carboxyl and epoxy. GO shows excellent electronic, chemical and mechanical properties, and exhibits great application potential in electronics or medicine. Nevertheless, there are few studies on the effect of GO on patients with respiratory disease, on the toxicity mechanism and on means or strategies to reduce the adverse effects of GO. Allergic asthma is a multiple risk factors induced chronic airway inflammation with high morbidity and mortality, and brings a significant adverse impact on the health of human life. The aim of this study is to explore the toxicity of GO and its mechanism through the allergic asthma mouse model, and provide experimental and theoretical basis for the safe application of GO in the future.In this study we focus on investigating whether graphene oxide (GO), a promising carbonaceous nanomaterial with unique physicochemical properties, aggravates allergic asthma in a mouse model. Mice were sensitized with ovalbumin (OVA) to trigger immune reactions, while vitamin E (Ve) was regarded as an antioxidant. Through the observation on lung histological sections (H&E staining, Masson staining, PAS staining), counting inflammatory cells (lymphocytes, eosinophils and neutrophils) in bronchoalveolar lavage fluid (BALF), and lung function measurement to evaluate the aggravating effect of allergic asthma in mice by GO exposure. Through the detection of oxidative stress indicators, including reactive oxygen species (ROS), malondialdehyde (MDA) and glutathione (GSH), and inflammation indicators, including interleukin-4 (IL-4), gamma interferon (IFN-y) and immunoglobulin E (IgE) to explore the possible mechanism of aggravation.The results showed that in the OVA combined with GO exposure groups, the level of oxidative stress in mice elevated, ROS and MDA content increased while GSH content decreased. The level of IgE also elevated after exposure. Inflammatory cytokines results revealed that the expression of IL-4 increased significantly and IFN-γ decreased significantly, suggesting the up-regulation of the Th2 response. In the meanwhile, the symptoms of allergic asthma aggravated in mice, such as the increasing number of lymphocytes, eosinophils and neutrophils in bronchoalveolar lavage fluid (BALF), airway remolding, collagen deposition together with mucus hypersecretion and airway hyperresponsiveness (AHR). The groups of GO 0.40 mg/kg+OVA and GO 4.00 mg/kg +OVA showed higher oxidative stress level and more severe allergic asthma symptoms. The administration of Ve after GO exposure dramatically attenuated all these effects.The results of this study demonstrated that GO could aggravate allergic asthma effects which have close correlation with oxidative stress in mice, the administration of Ve decreased the level of oxidative stress, as well as the degree of allergic asthma, indicating that GO aggravates allergic asthma in a mouse model via an oxidative stress pathway, and Ve showed anti-allergic properties in antagonizing the exacerbation of allergic asthma, providing a new possibility for the treatment of allergic asthma.