EFFECTS OF SALBUTAMOL, MONTELUKAST AND PREDNISOLONE AND THEIR COMBINATION ON LUNG TISSUE HISTOLOGY IN OVALBUMIN INDUCED ASTHMA IN FEMALE SPRAGUE DAWLEY RATS
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Abstract
Asthma is a chronic inflammatory airway disorder marked by bronchoconstriction, mucus hypersecretion, and infiltration of inflammatory cells. While current therapies such as salbutamol, montelukast, and prednisolone are effective in alleviating symptoms, their combined effects on lung tissue integrity remain unclear. This study evaluated the effects of salbutamol, montelukast, prednisolone, and their combinations on lung histology in ovalbumin (OVA)-induced asthmatic female Sprague-Dawley rats. Fifty-six adult female Sprague-Dawley rats were divided into five groups (n = 8): negative control, positive control (OVA-induced, untreated), salbutamol + prednisolone, salbutamol + montelukast, and prednisolone + montelukast. Asthma was induced through OVA sensitisationand aerosol challenge for four weeks. After confirming the development of asthma, treatment was administered orally for four weeks. Lung tissues were excised, fixed in 10% formalin, processed, and stained with hematoxylin and eosin (H&E) for histopathological evaluation under light microscopy. The negative control group showed normal lung architecture with intact bronchi and alveolar sacs. The OVA-induced positive control exhibited hyperplasia of bronchus- associated lymphoid tissue (BALT) and features of follicular bronchiolitis. The salbutamol/prednisolone and prednisolone/montelukast groups showed preserved lung structure with minimal inflammation and normal bronchi and alveolar spaces. In contrast, the salbutamol/montelukast group displayed marked bronchoconstriction and severe BALT hyperplasia, exceeding that seen in the untreated asthmatic group. Conclusion: Combination therapy with prednisolone and either salbutamol or montelukast effectively preserved lung histoarchitecture in OVA-induced asthmatic rats, indicating potent anti-inflammatory protection. However, the salbutamol/montelukast combination failed to reverse asthmatic histopathology, suggesting reduced therapeutic synergy or potential antagonistic interaction. These findings underscore the importance of drug selection in optimising asthma management and preventing structural lung damage.
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