Abstract
Synthetic therapeutic drugs for asthma, a chronic airway inflammation characterised by strong eosinophil, mast cell, and lymphocyte infiltration, mucus hyper-production, and airway hyper-responsiveness, exhibit numerous side effects. Alternatively, the high antioxidant potential of palm oil phytonutrients, including vitamin E (tocotrienol-rich fractions; TRF) and carotene, may be beneficial for alleviating asthma. Here, we determined the therapeutic efficacy of TRF, carotene, and dexamethasone in ovalbumin-challenged allergic asthma in Brown Norway rats. Asthmatic symptoms fully developed within 8 days after the second sensitization, and were preserved throughout the time course via intranasal ovalbumin re-challenge. Asthmatic rats were then orally administered 30 mg/kg body weight TRF or carotene. TRF-treated animals exhibited reduced inflammatory cells in bronchial alveolar lavage fluid. TRF- and carotene-treated rats exhibited notable white blood cell reduction comparable to that from dexamethasone. TRF- and carotene-treatment also downregulated pro-inflammatory markers (IL-β, IL-6, TNF-α), coincident with anti-inflammatory marker IL-4 and IL-13 upregulation. Treatment significantly reduced asthmatic rat plasma CRP and IgE, signifying improved systemic inflammation. Asthmatic lung histology displayed severe edema and inflammatory cell infiltration in the bronchial wall, whereas treated animals retained healthy, normal-appearing lungs. The phytonutrients tocotrienol and carotene thus exhibit potential benefits for consumption as nutritional adjuncts in asthmatic disease.
Highlights
Asthma constitutes a chronic inflammatory airway disease that is characterized by bronchial hyper-responsiveness owing to different stimuli, bronchoconstriction, airflow restriction, and inflammation of the bronchi causing coughing, wheezing, chest tightness, and dyspnea [1,2]
Allergic asthma is caused by allergens such as dust, pollen, and animal dander that trigger inflammation and initiate airway remodeling, which is characterized by deposition of reconditioned collagens, along with matrix protein damage owing to continuous inflammation and damage of the airway epithelium [2,5]
Th2 lymphocytes promote the release of interleukin (IL)-5 by eosinophils and IL-4 via immunoglobulin E (IgE) in mast cells [6]
Summary
Asthma constitutes a chronic inflammatory airway disease that is characterized by bronchial hyper-responsiveness owing to different stimuli, bronchoconstriction, airflow restriction, and inflammation of the bronchi causing coughing, wheezing, chest tightness, and dyspnea [1,2]. Airflow obstruction in asthma is preceded by bronchoconstriction, followed by mucosal edema, increased secretion of mucus, and infiltration of inflammatory cells into smooth muscle tissues with abundance of eosinophils in the bronchial mucosa, leading to excessive mucus secretion [3]. Histamine promotes bronchoconstriction, increasing vascular permeability and producing more mucus, whereas prostaglandin D2 triggers bronchoconstriction and leukotrienes concomitantly enhance vascular permeability, followed by mucus secretion and bronchoconstriction [9]. This late reaction includes the enrolment of mast cell and other effector cells, especially TH2 lymphocytes, eosinophils, neutrophils, and basophils, which are characteristic of asthma pathogenesis. Long term consumption of asthma controlled medications, such as anti-IgE or immunomodulators, by asthmatic patients was reported to cause development of anaphylaxis, platelet dysfunction, GI problems, acute renal failure, and edema [10]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
