Objective: To study the effect of charred Arteisia frigida on the change of mRNA expressions of vascular endothelial growth factors(VEGF)

basic fibroblast growth factors(bFGF) and their receptors in ulcer tissues of stress gastric ulcer model rats

and investigate the molecular mechanism for charred A.frigida to promote the healing of gastric ulcers. Method: 84 SD rats were randomly divided into 7 groups

named control group

model group

Yunnanbaiyao group(Positive drug

0.18 g·kg-1)

A.frigida crude drug group(1.35 g·kg-1)

low dose charred A.frigida group

middle dose charred A.frigida group and high dose charred A.frigida group(0.9

1.35

1.8 g·kg-1). Water-immersion stress method was used in all other groups except normal group to establish rat models of cute gastric ulcer. After intragastric administration for one continuous week

stomach ulcer tissues were scissored from the conventionally sacrificed animals. Western blot and RT-PCR technique were used to detect mRNA and protein expressions of VEGF and its receptor VEGFR

bFGF and its receptor bFGFR. Result: Compared with the normal group

ulcer tissues in rats with acute stress ulcer had significantly decreased bFGF(P<0.01) and bFGFR(P<0.05) protein expressions. Compared with the model group

charred A.frigida low dose group significantly increased VEGF mRNA expression(P<0.05)

VEGF protein expression VEGFR protein expression(P<0.05)

but without dose dependence; no difference was found between the other groups and the model group. charred A.frigida middle dose group

high dose group and Yunnanbaiyao group significantly increased bFGF protein expression(P<0.01)

and charred A.frigida high dose group also increased bFGF mRNA expression

bFGFR mRNA expression(P<0.01) and bFGFR protein expression(P<0.05). Conclusion: The molecular mechanism for charred A.frigida to promote the healing of gastric ulcers may be associated with up-regulation of VEGF and VEGFR protein expressions

bFGF and bFGFR protein expressions. The regulation of VEGF

bFGF

and bFGFR is at the level of transcription

and the regulation of VEGFR is at the post-transcriptional levels.