3, 3′-Diindolylmethane Attenuates Allergic Rhinitis by Subduing Interleukin-13-triggered JME/CF15 Human Nasal Epithelial Cells Inflammation

Allergic rhinitis (AR) is achronic, characteristic allergic syndrome that affects the upper airways of the nasal mucosa. The interleukin (IL)-13 signaling has been involved in the pathogenesis of AR. 3, 3 '-Diindolylmethane (DIM) is an antitumor bioactive component resulting from the acid-condensation product of indole-3-carbinol (I3C), originating in the Brassica vegetation. Although DIM is known for anti-inflammatory actions on many disorders, the role of DIM on AR is quiet unidentified. Hence, the current research was to consider the anti-inflammatory activities of DIM on IL-13 prompted in human nasal epithelial cells (HNECs). JME/CF 15 cells were pretreated with varied concentrations of DIM followed by IL-13 induced AR. In this study, we carried out in vitro analysis such as, cytotoxicity assay, ROS, apoptosis, inflammatory mediators, cytokines expressions of mRNA, and protein of DIM activity on HNECs cells were evaluated by CCK-8 assay, DCFH-DA, DAPI, ELISA, RT-qPCR, and western blot analysis. Our results found that DIM (5, 10, 20, and 30 mu M) showed anti-proliferative effects on the JME/CF 15 cells in a concentration-dependent manner. DIM noticeably reduces ROS, apoptosis, eotaxin, IL-8, IL-6, and GM-CSF established on DIM concentration. The outcomes propose that DIM may act as an anti-inflammatory agent to recover the AR symptoms by attenuating the nasal epithelial inflammatory response.