Bacoside A Averts Oxidative Stress and Inflammation in Pulmonary Disease Induced by Cigarette Smoke in Rats Through NRF2/ATF4 and TLR4/NF-κB Signaling Pathways

Background

Chronic Obstructive Pulmonary Disease (COPD) has emerged as a foremost cause of worldwide illness. Exposure to Cigarette Smoke (CS) contributes to Oxidative Stress (OS) and inflammation, which is a chief cause of COPD.

Objectives

Bacoside A (BA) is a triterpenoid saponin extracted from the plant Bacopa monnieri (Brahmi), renowned as a potent nerve stimulant, exerting antioxidant, anti-inflammatory, and anticancer activities.

Materials and Methods

Previously, it has been investigated that BA acts as a neuroprotective agent in CS-induced brain damage in rats. Hence, this current study assessed the protective effect of BA in relieving lung inflammation and Oxidative Stress (OS) caused by CS-triggered COPD. Albino rats were disseminated into 5 sets: sham, CS-induced, CS+BA (5 mg/kg bw), CS+BA (10 mg/kg bw), and CS+BA (15 mg/kg bw). COPD was developed to assess breathing capacity, inflammatory cells in BALF, OS markers, cytokines, histopathology, and western blot.

Results

BA dose-dependently alleviates the OS, MDA, cytokines, inflammatory cells, and histopathological variations, while enhancing antioxidant status in COPD-stimulated rats.

Conclusion

Our data exhibited that BA could protect against COPD in CS-stimulated rats by suppressing inflammation and OS in the lungs by modulating the TLR4/NF-κB and Nrf2/ATF4 signalling pathways.