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Baisakhi Moharana, Ph. D.

Scientist,Pharmacology

Understanding the pharmacological basis and therapeutic interventions in the area
of Chronic Obstructive Pulmonary Disease (COPD), lung carcinogenesis, airway
inflammatory disorders, and associated cardio-pulmonary complications




Chronic obstructive pulmonary disease (COPD) is one of the foremost prevalent respiratory illness, crucially associated with persistent symptoms including small airway obstruction, chronic pulmonary inflammation, and pulmonary emphysema. Cigarette smoking and air pollution are major risk factors identified as significant initiator of pathology in COPD. Chronic inflammation during COPD pathogenesis is specified by increased CD4+ and CD8+ cells and accumulation of alveolar macrophages, neutrophils and T-lymphocytes. Proteases, free radicles and cellular mediators secreted from the activated immune cells has been incriminated in all aspects of COPD, implicated in surrounding tissue demolition, decline in lung plasticity, hyper-mucous secretion resulting in to emphysema and chronic bronchitis in COPD. Increasing evidences suggests that imbalance between oxidative and anti-oxidative factors play pivotal role in all facets of pathogenesis of COPD.

Other research areas:

➤ Regulatory Safety Pharmacology (Respiratory studies)
➤ Asthma and airway inflammation
➤ Cardio-metabolic Disorders
➤ Lung carcinogenesis
➤ Ethno pharmacology and therapeutic exploration of phyto-components

Current Lab focus:

Our lab has standardized COPD model both in vitro and in vivo using reference grade 3R4F cigarettes (The Tobacco and Health Research Institute, University of Kentucky, USA). We have established the effect of cigarette smoke on ageing by treating the 12-14 months’ rats with cigarette smoke extract and observed in our study that cigarette smoke induces neoplastic changes along with fibre deposition in lungs. We found that, prolonged cigarette smoke extract exposure worsens the respiratory functions including alteration in tidal volume (TV) and enhanced pause. Major molecular signalling pathway including wnt3a-β-catenin signalling and Tweak-Fn14 signalling has been explored in the pathogenesis of COPD. Our research group is also involved in screening and development of new therapeutic interventions in experimental model of asthma, airway inflammatory disorders and cardio-metabolic disorders.