Study on Therapeutic Effect and Mechanism ofQi-Zhu Er-Zhu Er-CaoTang in Treatment of Chronic Atrophic Gastritis Precancerous Lesion Based on Pathway of NF-κB (p65) and CyclinE / 世界科学技术-中医药现代化

ABSTRACT

This study was aimed to observe the therapeutic effect and mechanism ofQi-Zhu Er-Zhu Er-Cao Tang(QZEZECT) in the treatment of chronic atrophic gastritis (CAG) precancerous lesion. A total of 56 clean grade healthy Wistar rats were randomly divided into 6 groups. In the negative control group (NC), model group,Wei-Fu-Chun(WFC) group,Ren-Zhu Jian-Wei Ke-Li(RZJWKL, RZ) group, there were 10 rats in each group. In the high-dose QZEZECT (QZ-H) group and low-dose QZEZECT (QZ-L) group, there were 8 rats in each group. CAG/PLGC model was established by MNNG in the model group, WFC group, RZ group, QZ-H group and QZ-L group. Intragastric administration of corresponding decoctions at the dose of 0.39 g·kg-1, 3.2 g·kg-1, 54.4 g·kg-1, 13.6 g·kg-1 were given to rats in the WFC, RZ, QZ-H and QZ-L groups once a day for 28 consecutive days, respectively. The same volume of normal saline was given to the NC group and the model group. Histomorphological changes of gastric mucous membrane in rats of each group were observed. Expressions of NF-κB/p65 and CyclinE protein were detected. The results showed that compared with the NC group, the degrees of infiltration and dysplasia and expressions of NF-κB/p65 and CyclinE significantly increased in the model group with statistical significance (P < 0.01). Compared with the model group, the expression of NF-κB/p65 and CyclinE in the WFC group reduced with statistical significance (P < 0.05). The expression of NF-κB/p65 and CyclinE in the RZ and QZ-L group obviously reduced with statistical significance (P < 0.01). The overall effective rates of WFC group, RZ group, QZ-H group and QZ-L group were 50%, 63.3%, 43.3% and 73.3%, respectively. It was concluded that QZEZECT can treat CAG precancerous lesion, which may take effect by improving and inhibiting pathologic changes of the transcription factor of inflammation.