Epigallocatechin gallate protects BEAS-2B cells from lipopolysaccharide-induced apoptosis through upregulation of gastrin-releasing peptide

Abstract

Gastrin-releasing peptide (GRP) plays a major role in the development and maintenance of lung epithelial cells by promoting cell division, whereas its suppression causes growth arrest and apoptosis. The present study shows that human bronchial epithelial BEAS-2B cells challenged with lipopolysaccharide (LPS), an endotoxin from gram-negative bacteria, downregulated GRP expression and induced apoptosis via upregulation of p53 and active caspase-3, signifying the importance of GRP in lung epithelial cell survival. However, in the presence of epigallocatechin-3-gallate (EGCG), a polyphenol in green tea, BEAS-2B cells resisted LPS-induced apoptosis and restored the expression of GRP and its downstream effectors such as epidermal growth factor receptor and NF-κB, as analysed by immunoblotting and qPCR. Based on our findings, we objectify that cytoprotective functions of EGCG, via upregulation of GRP in cells challenged with LPS, are novel and can be further explored in a therapeutic point of view for diseases such as septic shock.

Amygdalin Attenuates Airway Epithelium Apoptosis, Inflammation, and Epithelial-Mesenchymal Transition through Restraining the TLR4/NF-κB Signaling Pathway on LPS-Treated BEAS-2B Bronchial Epithelial Cells

“…Similarly, following the establishment of CVA models, we found that treatment with amygdalin at lower than 400 μg/mL promoted the toxicity of CVA model cells. Besides, both airway epithelial inflammation and dysfunction in allergic asthma and exposure to LPS were found to induce cell apoptosis [29,30]. Analogously, our study demonstrated an apoptosis-inducing effect of LPS.…”

Combination of green tea catechins, polysaccharides, and flavonols against urban fine dust particle-induced bronchial damage mediated by modulation of inflammation factors and airway cilia

“…The human bronchial epithelial cell line BEAS-2B (CRL-9609), the human broblast cell line IMR90 (CCL-186), and the human lung adenocarcinoma cell line A549 (CCL-185) were purchased from the American Type Culture Collection (ATCC, Manassas, VA, USA). The BEAS-2B cells were cultured in 25 mM HEPESbuffered M199 medium containing 10% FBS, 2 mM L -glutamine, 100 U/ml penicillin, 100 mg/ml streptomycin supplemented with 2.5 mg/ml insulin, 361 ng/ml hydrocortisone, 2.5 mg/ml apotransferrin, and 20 ng/ml EGF [86]. The IMR90 cells were maintained in Eagle's MEM (EMEM, Lonza 125F) supplemented with 2 mM L -glutamine, 10% FBS and 1 mM sodium pyruvate with 100 U/ml penicillin and 100 mg/ml streptomycin.…”