HBE135-E6E7

Acacetin Elevated Cell Viability and Alleviated Oxidative Stress Damage in CSE-Treated HBE135-E6E7 Cells

Chronic obstructive pulmonary disease (COPD) is a leading cause of death globally, with cigarette smoke being a major cause. Acacetin has shown lung-protective effects, but its role and mechanism in COPD are unclear. Chen's team explored how Acacetin protects human bronchial epithelial cells from cigarette smoke extract (CSE)-induced injury through the NRF2/SLC7A11/GPX4 signaling pathway.

They first investigated the effect of CSE on cell viability in HBE135-E6E7 cells. The results showed that CSE significantly reduced cell viability in a dose-dependent manner (Fig. 1A). Then the levels of LDH in the medium were measured as an injury index of cells. The results showed that LDH in the medium was increased in a dose-dependent manner by CSE (Fig. 1B). On this basis, 5% CSE was used in the following experiments. They then determined the influence of Acacetin on cell viability. As shown in Fig. 1C, Acacetin (12.5, 25, or 50 μg/ml) alone had no significant effect on cell viability. Acacetin significantly alleviated the decrease of cell viability caused by CSE in a dose-dependent manner (Fig. 1D). The results of LDH showed that Acacetin reduced LDH in the medium and suggested alleviation of cell injury (Fig. 1E). Acacetin decreased the generation of ROS in a dose-dependent manner (Fig. 1F). In addition, Acacetin attenuated CSE-induced MMP loss (Fig. 1G).

The IRE1α Inhibitor, 4μ8C, Exerts Suppressive Effects on the PM2.5-Induced Apoptosis of Airway Epithelial Cells

Fine particulate matter (PM2.5) is a major air pollutant that can cause airway inflammation. Hu's team investigated the effects of PM2.5 on endoplasmic reticulum (ER) stress and airway inflammation in human airway epithelial cells, specifically focusing on the role of the IRE1α/NOD1/NF‑κB pathway in these processes.

To identify the appropriate concentrations and time durations of PM2.5 for the study, HBE135-E6E7 cells were treated with different concentrations of PM2.5 for different time periods. The viability of cells was determined by CCK-8 assay. The viability analysis demonstrated no significant differences between the control and PM2.5-treated groups (10-100 μg/ml) at 12 and 24 hours but showed decreased viability in the 200 and 400 μg/ml groups from 12 to 48 hours and in 10-100 μg/ml groups at 48 hours. (Fig. 2). To explore whether PM2.5 can activate ER stress pathway, the expression of the proteins associated with ER stress was measured after PM2.5 treatment. Western blot was performed to detect the levels of proteins including GRP78, CHOP, p-IRE1α, NOD1, ATF6 and p-PERK. As shown in Fig. 3, exposure to 100 μg/ml PM2.5 for 24 h, significantly increased the expression of these proteins compared to the control group. However, 4-PBA, an ER stress inhibitor pre-treatment significantly inhibited the expression of these proteins compared to PM2.5 only treated group (Fig. 3).