Acute exposure of ozone induced pulmonary injury and the protective role of vitamin E through the Nrf2 pathway in Balb/c mice

Abstract

Ozone (O) in the lower atmosphere is generally derived from various sources of human activity. It has become a major air pollutant in China and has been shown to adversely affect the health of humans and animals. We undertook a study to ascertain the molecular mechanism of ozone induced lung injury in mice and tried to demonstrate the protective mechanism of vitamin E. In this study, mice were exposed to clean air and three different concentrations of ozone. Oxidative stress (reactive oxygen species and malondialdehyde) and Th cytokines in the lung, serum IgE, as well as histopathological examination and the airway hyper-responsiveness (AHR) test were used to reflect inflammation and damage to the lungs of ozone-exposed mice. We then chose an effective concentration of ozone and combined treatment with vitamin E (VE) to explore the underlying mechanism of ozone-induced lung damage. The results of immunological and inflammatory biomarkers (total-immunoglobulin (Ig) E and Th cytokines) as well as histopathological examination and AHR assessment supported the notion that high doses of ozone (>0.5 ppm) could induce inflammation and lung injury in mice and that this induction was counteracted by concurrent administration of VE. The elimination of oxidative stress, the reduced Th2 responses and Ig production, and the relief of lung damage were proposed to explain the molecular mechanism of ozone induced lung injury. We also showed that VE, an antioxidant that enhanced the expression of Nrf2 and up-regulated the antioxidant genes HO-1 and NQO1, could decrease the levels of oxidative stress and alleviate ozone-induced lung injury.

ERK1/2 and p38 regulate inter-individual variability in ozone-mediated IL-8 gene expression in primary human bronchial epithelial cells

“…This is suggested by the fact that even when both p38 and ERK1/2 inhibitors were used, we did not achieve a complete reduction of expression; moreover, IL-8 inductions in low responders were not influenced by kinase inhibition. This residual IL-8 induction may be due to low-level inputs from other cellular effectors, such as NRF2 30 .…”

Serum level and clinical significance of vitamin E in children with allergic rhinitis

“…Vitamin E, a essential nutrient for reproduction, is synthesized in plant organisms and composed of eight fat-soluble compounds(α-, β-, γ-, δ-tocopherol, and α-, β-, γ-, δ-tocotrienol) [ 6 ].Some studies have confirmed that oxidative stress plays an important role in the pathogenesis of several allergic diseases, including AR [ 7 ]. Vitamin E is a peroxyl radical scavenger that can protect neurons and respiratory mucosa from oxidant damage, while vitamin E can significantly reduce the incidence of asthma and relieve respiratory mucosa inflammation [ 8 , 9 ].…”

Dermal exposure to nano-TiO₂ induced cardiovascular toxicity through oxidative stress, inflammation and apoptosis

“…Vit E has the effect of scavenging free radicals because its phenolic hydroxyl group can donate hydrogen atoms (Lu et al, 2011), and is thus very likely to reduce ROS levels, ameliorate inflammation and control apoptosis. Also, studies have demonstrated that Vit E can trigger an antioxidant pathway, such as the nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway, and provide antioxidant benefits (Zhu et al, 2015). Furthermore, Vit E can play a protective role in cardiovascular health by controlling the levels of adhesion molecules, reducing the activation of monocytes or macrophages, and down-regulating the proliferation of smooth muscle cells (Mocchegiani et al, 2014).…”