Objective: To investigate the effect and mechanism of baicalin in alleviating Helicobacter pylori(Hp)-induced human gastric epithelial GES-1 cells injury. Method: baicalin (15

30

60 mg·L-1) or a specific inhibitor of p38 MAPK pathway SB203580 20 μmol·L-1 was added into Hp-infected GES-1 cells. Proliferation and apoptosis

levels of interleukin-1β (IL-1β) and IL-8

lactic dehydrogenase (LDH) activities

protein expressions of B-cell lymphoma-2(Bcl-2) associated X protein(Bax)

Bcl-2

p-p38 MAPK and total-p38 MAPK(T-p38 MAPK) in GES-1 cells were determined by MTT assay

flow cytometry

ELISA

colorimetry and Western blot

respectively. Result: Compared with control group

Hp significantly inhibited proliferation of GES-1 cells

increased apoptosis

LDH activities

IL-1β and IL-8 levels

Bax and p-p38 MAPK expressions

but decreased Bcl-2 expression in GES-1 cells (P<0.01). Compared with Hp-infected GES-1 cells

medium-dose and high-dose baicalin significantly increased proliferation of GES-1 cells

decreased apoptosis

LDH activities

IL-1β and IL-8 levels

Bax and p-p38 MAPK expressions

but increased Bcl-2 expression in GES-1 cells (P<0.01). Compared with the high-dose baicalin group

SB203580 significantly increased proliferation of GES-1 cells

decreased apoptosis

LDH activities

IL-1β and IL-8 levels

Bax and p-p38 MAPK expressions

but increased Bcl-2 expression in GES-1 cells (P<0.05

P<0.01). Conclusion: baicalin alleviated Hp-induced human gastric epithelial GES-1 cells injury through anti-inflammation

proliferation promotion and anti-apoptosis. The mechanism may be correlated with the inhibition of p38 MAPK signaling pathway.