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

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-jB,
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.