Naringenin attenuates inflammation in chronic obstructive pulmonary disease in cigarette smoke induced mouse model and involves suppression of NF-κB.

Inflammation of lungs and airways is a primary symptom of the Chronic Obstructive Pulmonary Disease (COPD). The COPD inflammation is known to be mediated by several factors such as pro-inflammatory cytokines, glucocorticoid receptor (GR), NF-κB. Patients with COPD respond very poorly to the corticosteroid therapy. Naringenin is a flavonoid known to possess anti-inflammatory properties. We studied the effect of naringenin on COPD induced due to cigarette smoke (CS) in BALB/c mouse model and in vitro in A549 cells. COPD was induced in Mice by exposing them to CS for 90 days. The animals were pre-treated with naringenin in 20, 40 and 80 mg/Kg concentration. Whereas, the in vitro cells were treated with naringenin along with CS extract exposure. Naringenin was found to significantly improve the pulmonary function, decreased inflammatory cells, and inhibited the production of pro-inflammatory cytokines such as IL-8, TNF-α, and MMP9 in the BALF and serum of CS animal group. Naringenin also appeared to inhibit the NF-κB pathway as revealed by reduced phosphorylation of NF-κB and IκB in western blot test. Moreover, the levels GR mRNA and protein were also significantly increased upon treatment with naringenin to CS-exposed animals and cell culture. It could be concluded that naringenin can be a potential therapeutic agent for the treatment of COPD-related inflammation.