Beta-elemene alleviates cigarette smoke-triggered inflammation, apoptosis, and oxidative stress in human bronchial epithelial cells, and refrains the PI3K/AKT/mTOR signaling pathway.

Background: Chronic obstructive pulmonary disease (COPD) is a grievous disease that adversely affects human health and life. β-elemene is a type of sesquiterpenoid extracted from Curcuma wenyujin (Zingiberaceae) and displays effects on suppressing tumor growth. However, the regulatory impact of β-elemene in COPD development is not reported.

Objective: This study explored the functioning of β-elemene in the progression of COPD.

Material and methods: The cell survival rate was confirmed through Cell Counting Kit-8 (CCK-8) assay. The cell apoptosis was evaluated through flow cytometry. The protein expressions were examined through western blot. The levels of malondialdehyde (MDA), superoxide dismutase (SOD) and reactive oxygen species (ROS) were examined through the corresponding commercial kits. The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1β were inspected through Enzyme-Linked Immunosorbent Assay (ELISA).

Results: The study demonstrated that β-elemene exaggerated cell viability and reduced cell apoptosis in BEAS-2B human bronchial epithelial cell line stimulated by cigarette smoke extract (CSE). Oxidative stress was heightened after 5% CSE induction, but this impact was counteracted by β-elemene treatment. In addition, enhancive inflammation induced by cigarette smoke was attenuated by β-elemene treatment. Finally, our results indicated that the triggered the phosphatidylinositol 3-kinase-protein kinase B-mechanistic target of rapamycin (PI3K/AKT/mTOR) pathway mediated by cigarette smoke was refrained by β-elemene treatment.

Conclusion: It was concluded that β-elemene reduced cigarette smoke-triggered inflammation, apoptosis, and oxidative stress in human bronchial epithelial cell line, and refrained PI3K/AKT/mTOR signaling pathway. This study proposed that β-elemene could act as a hopeful drug for the treatment of COPD.