Abstract:
OBJECTIVE To observe the effect of Weifuchun on interleukin-6(IL-6)/Janus protein tyrosine kinase 2(JAK2)/signal transducer and activator of transcription 3(STAT3) signaling pathway in gastric mucosal tissues of model rats with
Helicobacter pylori(Hp) infection complicated with chronic atrophic gastritis(CAG).
METHODS Totally 45 healthy male rats were selected and randomly divided into the blank control group with 12 rats and the modeling group with 33 rats. The model was established by gavage of Hp suspension and mixture of sodium salicylate and ethanol. The model of Hp infection with CAG was observed at the end of the 14 th week of modeling, the rats of the model group were randomly divided into the control group, the high-dose group and the low-dose group after the successful modeling. The model control group was given 10 mL/kg normal saline by gavage, and the high-dose group was given 1.56 g/kg Weifuchun by gavage, and the low-dose group was given 0.78 g/kg Weifuchun by gavage, and the blank control group was only fed normally, and all rats were given 4 weeks of administration. The positive rate of Hp culture, pathological scores, messenger ribonucleic acid(mRNA) relative expression levels of IL-6, JAK2, STAT3 and nuclear factor-κB(NF-κB) in gastric mucosal tissues were compared among the four groups.
RESULTS The positive rate of Hp in gastric mucosal tissues of the three modeling groups was significantly higher than that of the blank control group(
P<0.05). The pathological scores of gastric antrum and gastric body mucosal tissues and mRNA relative expression levels of gastric mucosal tissue IL-6, JAK2, STAT3 and NF-κB were significantly higher in the three modeling groups than in the blank control group(
P<0.05), which were significantly higher in the model control group than in the high-dose group and the low-dose group, significantly higher in the low-dose group than in the high-dose group(
P<0.05).
CONCLUSION Weifuchun can achieve remarkable therapeutic effect on the rats with Hp infection and CAG, and the action mechanisms may be related to its inhibition of expression of IL-6/JAK2/STAT3 signaling pathway and NF-κB.