Abstract
Purpose: To determine the therapeutic effect of coenzyme Q10 (CoQ10) on ovalbumin (OVA)-provoked asthma in neonatal rats.Methods: Asthma was induced by exposing neonatal rats to OVA. The levels of SOD, CAT, GPx, GSH, MDA and MPO were estimated using standard biochemical kits, while ELISA was used to measure the concentrations of Ig E and Th2 cytokines. Gene expressions were assayed with qRT-PCR, and protein expressions were determined with western blotting.Results: OVA treatment led to increases in levels of BALF inflammatory cells, lipid peroxidation, serum IgE and BALF Th2 cytokines, but it decreased antioxidant levels. Furthermore, the protein expression of NF-κB and mRNA expression levels of proinflammatory cytokines and inducible nitric oxide synthase (iNOS) were upregulated in the asthmatic rats (p < 0.05). However, coenzyme Q10 supplementation significantly decreased lipid peroxidation, and reduced inflammatory cells and IgE levels, while the antioxidant levels were enhanced (p < 0.05). Moreover, coenzyme Q10 reduced the levels of Th2 cytokines and downregulated the expressions of NF-κB, TNF-α, IL-6, and iNOS in the neonatal asthmatic rats (p < 0.05).Conclusion: Coenzyme Q10 attenuates airway inflammation and oxidative stress in neonatal asthmatic rats. Thus, coenzyme Q10 has promising therapeutic potential in the management of asthma.
 Keywords: Asthma, Neonatal, Coenzyme Q10, Th2, cytokines, Oxidative stress, Antiinflammation
Highlights
Asthma is a long-term inflammatory and allergic airway pathology caused by infiltration of immune cells such as neutrophils, lymphocytes and macrophages into the lung tissues [1]
The Th2 cytokines implicated in asthma are IL-4, IL-5 and IL-13, with IL-4 as the important mediator involved in the maturation of Th2 cells, allergic reactions and IgE release [4]
Administration of Coenzyme Q10 (CoQ10) to the asthmatic rats significantly reduced the oxidative stress by increasing the levels of antioxidants
Summary
Asthma is a long-term inflammatory and allergic airway pathology caused by infiltration of immune cells such as neutrophils, lymphocytes and macrophages into the lung tissues [1]. The other clinical factors involved in asthma are high concentrations of IgE, infiltration of mast cells as a result of inflammation, and aggravated release of cytokines and chemokines. These factors result in accumulation of the inflammatory cells in the airway area, leading to generation of toxic free radicals. The Th2 cytokines implicated in asthma are IL-4, IL-5 and IL-13, with IL-4 as the important mediator involved in the maturation of Th2 cells, allergic reactions and IgE release [4]. A viable therapeutic option is the treatment/prevention of asthma using alternative medicine
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