Emodin Attenuates Ozone-Induced Lung Injury Via TLR4/MYD88/NF-κB Signaling Pathways

In defense of the internal and external environment of the lung airway, airway epithelial cells play important roles in resisting external microorganisms, toxic gases, sensitizing substances, and maintaining the stability of the internal environment of the airway. C57Bl/6 mice were exposed to ozone for 4 days (30 min/day) to induce lung injury. Airway responsiveness was measured using barometric whole-body plethysmography. Hematoxylin and eosin (HE) staining was used to detect pathological changes of the lung. Bronchoalveolar lavage (BAL) was performed to count the number of macrophages and neutrophils. 16HBE14o- cells were exposed to ozone for 30 min. 3-[4,5-dimethylthiazolyl-2]-2,5-diphenyltetrazolium bromide was used to detect cell proliferation. Reactive oxygen species (ROS), lactate dehydrogenase (LDH), and catalase (CAT) in lung tissues and cells were also measured. The mRNA and protein expressions were detected by qPCR and western blot. We found that emodin attenuated ozone-induced airway hyperresponsiveness and lung inflammation in vivo. Emodin reduced the production of ROS, increased the expression of antioxidant enzymes, and attenuated the oxidative damage in vivo. In vitro studies showed that emodin also decreased ROS generation and LDH release and enhanced CAT activity. Emodin attenuates ozone-induced TLR4, MyD88, and NF-eB expression. Emodin has anti-inflammatory and antioxidant properties through the modulation of the TLR4-MyD88-NF-eB pathway in ozone-induced lung injury.