EFFECT OF BAICALEIN ON PCNA EXPRESSION DURING THE DEVELOPMENT OF MURINE FORE- STOMACH CARCINOMA

LU PING, SHI BO

School of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, China

Introduction: To investigate the effect of baicalein on Proliferating cellular nuclear antigen (PCNA) expression in dynamic process of murine fore-stomach carcinoma.

Materials and methods: Dynamic animal models of murine fore-stomach carcinoma were established with the equal volume mixing (abbreviated as NSEE) of Sacrosine-ehylester-hydrochlorid and Sodium nitrite as a mutagen. 90 NIH mice (SPF) was divided into blank control group, the negative control group, high (1000mg kg-1), medium (500mg kg-1) and low (200mg kg-1) dose groups with baicalein (dissolved with 0.5% sodium carboxymethyl cellulose solution). In the experiment,all group were treated with NSEE, twice a week for six weeks by gavage,without the blank group (with equal volume of 0.9% saline). Meanwhile, all interventional groups with Baicalein were treated with baicalein solution by gavage once a day. The fore-stomach tissues were taken on 28th, 5 6th and 84th day for pathological observation. The PCNA expression in the fore-stomach tissues was observed by immunohistochemistry.

Results: Compared with the blank control group, for interventional group,fore-stomach tissues was gradually evolves from hyperplastic lesions to atypical hyperplasia,or even carcinoma in situ,and the PCNA expression in the negative control group increa- ses significantly (P <0.01) by immunohistochemistry. Compared with the negative control group,the situation is the slightest in high dose group by pathological sections at 84d, the experimental results by immunohistochemistry showed that PCNA expression of high,medium and low dose baicalein intervention groups was significantly different from that of model group (P <0.01), but there was no significant difference among the groups.

Conclusion: High, medium and low doses of baicalein can significantly inhibit NSEE-induced fore-stomach cancer carcinogenesis in mice, which may be related to down-regulation of PCNA expression.