Overweight and obesity are related to an increased risk of asthma. The effect of platycoside E (PE) on obesity-related asthma remains unknown.
To mimic obesity-related asthma conditions in vivo, C57BL/6 mice were exposed to a high-fat diet (HFD) and challenged with ovalbumin (OVA). PE was administrated intraperitoneally during the OVA treatment. Body weight was measured at 8th week before PE treatment and after sacrificing the mice. Airway inflammation and airway hyperresponsiveness (AHR) were evaluated. Immunohistochemistry staining was performed to evaluate eosinophils. Histopathological changes were determined by HE staining. Cellular model of asthma was established using IL-13 in BEAS-2B cells. Levels of proinflammatory cytokines and oxidative stress indicators were measured by ELISA kits and commercial kits, respectively. Cell viability was detected by CCK-8 assays.
IL-13 treatment led to inflammatory and oxidative damage in bronchial epithelial cells, which was relieved by PE. PE administration significantly reduced HFD-induced obesity and relieved AHR and airway inflammation in obese asthmatic mice. The expression of proinflammatory cytokines in BALF and lung tissues in obese asthmatic mice were reduced by PE. PE administration also reduced infiltration of eosinophils and inflammation scores in obese asthmatic mice.
PE suppresses airway inflammation and AHR in obese asthmatic mice and serves as an effective option for treating obesity-related asthma.

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