DR E.O ALOAMAKA

EFFECTS OF SALBUTAMOL , MONTELUKAST AND PREDNISOLONE AND THEIR COMBINATION ON SERUM OXIDANT AND ANTIOXIDANTS ENZYMES ACTIVITIES IN OVALBUMIN INDUCED SPRAGUE-DAWLEY RATS.

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Abstract
Asthma is characterized by chronic inflammation of the lower respiratory tract, a state frequently seen alongside inflammatory disorders of the upper airway (Mims, 2015). The 1995 GINA guidelines classified a patient's off-treatment asthma status (intermittent to severe persistent) to guide initial therapy. However, modern guidelines have abandoned this severity-based classification in favor of a focus on achieving and maintaining disease control. Current clinical practice defines asthma severity by the level of pharmacological treatment required to keep the disease controlled; in the most difficult cases, severity is determined by the condition's refractoriness to therapy(Song et al., 2019). Asthma is typically suspected based on a patient's recurring symptoms and their positive response to a bronchodilator medication, which helps relax the airway muscles(Sockrider and Fussner, 2020). For individuals over the age of five, the diagnosis is usually confirmed with a breathing test called spirometry (a type of pulmonary function test or PFT), which detects airway narrowing or obstruction. However, a normal spirometry result does not rule out asthma(Sockrider and Fussner, 2020). First-line asthma medications include the short-acting β2-adrenergic agonist salbutamol for rapid relief of bronchoconstriction, the leukotriene receptor antagonist montelukast for its anti-inflammatory and bronchodilatory effects, and the corticosteroid prednisolone for potent anti-inflammatory action(Whirledge and Cidlowski, 2010), these drugs exert their effects through different mechanisms, including bronchodilation, anti inflammatory actions, and inhibition of leukotriene-mediated inflammation (Barnes, 2008). The induction of airway inflammation using Ovalbumin (OVA) in Sprague-Dawley rats serves as a widely recognized model for studying asthma (Kumar and Herbert, 2013). This model triggers a Th2-mediated inflammatory response, which subsequently elevates the production of reactive oxygen species (ROS), resulting in oxidative stress (Rahman andMacNee, 2000)
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