Paclobutrazol ameliorates cigarette smoke-induced chronic obstructive pulmonary disease (COPD) in experimental rats

Background: The cigarette smoking epidemic is one of the desperate threats experienced all over the world. Cigarettes cause diseases such as chronic obstructive pulmonary disease (COPD), asthma, lung cancer, stroke, heart diseases, etc. Paclobutrazol is a growth regulator hormone that increases antioxidant enzymes, mineral absorption, carbohydrate synthesis, and flowering and fruit production in plants. Objective: In the current study, we assessed the ameliorative effect of paclobutrazol against chronic cigarette smoke-induced COPD in rats. Methodology: A side-stream cigarette exposure rat model was used for the study, which is a well-accepted model to evaluate cigarette smoke-induced lung damage. The paclobutrazol treatment was given for 12 weeks, and since the reduction in body weight is the primary symptom of COPD, the food efficiency and the weight gain were measured. Muscular strength was analyzed with a grip strength test, and respiratory functions were assessed with a whole-body plethysmograph. Plasma leptin was measured to detect the fat mass index. C-reactive protein was quantified to assess the level of inflammation. Further bronchoaleveolar fluid was collected and analyzed for the total white blood cell count, neutrophils, lymphocytes, and monocytes to evaluate the inflammation. In order to confirm the anti-inflammatory property of paclobutrazol against cigarette smoke-induced lung inflammation, histopathological analysis of lung tissue was done. Results: The paclobutrazol treatment increased the body weight, improved respiratory func-tions, and decreased inflammation in the rats exposed to secondhand cigarette smoke. Our results of histopathological analysis confirm that paclobutrazol has effectively inhibited cigarette smoke -induced lung tissue damage in young Wistrar rats. Conclusion: Hence, it can be used as a supplementary drug to protect smokers from cigarette smoke-induced lung damage. (c) 2023 The Authors. Published by Elsevier B.V. on behalf of King Saud University. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).