Potential anti-inflammatory and immunomodulatory effects of carvacrol against ovalbumin-induced asthma in rats.

Research paper by Yousra M YM Ezz El-Din, Ali A AA Aboseif, Marwa M MM Khalaf

Indexed on: 29 Oct '21Published on: 28 Dec '19Published in: Life Sciences


Asthma is a complex inflammatory disease which affects multiple individuals worldwide especially pediatric ages. This study aimed to assess the possible protective effect of carvacrol, as natural antioxidant anti-inflammatory drug, against bronchial asthma induced experimentally in rats. Rats were randomly allocated into 5 groups; a normal control group, control drug group received only carvacrol, an asthma control group, a standard treatment group receiving dexamethasone (DEXA) and carvacrol treatment group. Bronchial asthma was induced by sensitization with i.p dose followed by challenge with intranasal dose of ovalbumin (OVA). 24 h after the last challenge, absolute eosinophil count (AEC) were determined in bronchoalveolar lavage fluids (BALF). Immunoglobulin E (IgE) was determined in serum. Inflammatory biomarkers like Interleukin-4 (IL-4), interleukin-5 (IL-5), interleukin 13 (IL-13), tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ) were also measured in BALF. Nitrosative stress biomarker namely inducible nitric oxide synthase (iNOS) was determined in BALF as well as oxidative stress biomarkers namely superoxide dismutase (SOD), glutathione (GSH) and malondialdehyde (MDA) were determined in lung tissue. Additionally, histopathological study, immunohistochemical study of UCN and western blot analysis of SP-D were performed. Carvacrol administration significantly reduced the values of AEC, IgE, IL-4, IL-5, IL-13, TNF-α, IFN-γ, iNOS and MDA, while it significantly increased the values of SOD and GSH as compared to the asthmatic group. Histopathological, immunohistochemical and western blot study reinforced the biochemical results. Carvacrol may be a promising protective agent against bronchial asthma induced experimentally in rats. Copyright © 2019. Published by Elsevier Inc.