Use of Cnicin, a sesquiterpene lactone, as a treatment for lung inflammation in COPD

Chronic obstructive pulmonary disease (COPD) is characterized by an inflammatory condition mainly caused by cigarette smoke. In this heterogeneous disease, the underlying inflammatory process leads to progressive airflow obstruction, with recurrent acute exacerbations. Current treatments focus on slowing down the progress of the disease and mitigating the risks of exacerbations via administration of bronchodilators and steroids, that target both airways tightening and the underlying inflammation. However, for many patients, these treatments are not effective, creating a need for new therapies to be developed. Sesquiterpene lactones (STL) are secondary metabolites that have shown various pharmacological properties. Different structure-activity relationships have been drawn to explain these effects, most associated with alkylating structures. One of these compounds is Cnicin, a STL that has shown anti-inflammatory effect by the inhibition of nuclear factor-kappa-lightchain-enhancer of activated B cells (NF-kB). NF-kB, a family of inducible transcription
factors which regulates the development and progression of inflammation by the activation of proinflammatory genes encoding cytokines and chemokines and regulates cell survival and differentiation, is a transcription factor that plays a central role in inflammatory diseases like COPD and is strongly inhibited by Cnicin [4]. In this study, we investigate the anti-inflammatory potential of Cnicin in treating lung inflammation.