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Archive > Volume 32 Issue 4 > 2025,32(4):392-397. DOI:10.3872/j.issn.1007-385X.2025.04.007 Prev Next
Basic Research
The intervention of Jianpifuwei granule on mucosal injury of precancerous lesion of gastric cancer via the IL-6/JAK/STAT3 axis and its mechanisms
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Abstract:
[Abstract] Objective: To explore the intervention effect of Jianpifuwei granule (JPFWG) on gastric mucosal injury in rats with precancerous lesions of gastric cancer (PLGC) by regulating the IL-6/JAK/STAT3 signaling pathway and its mechanism. Methods: The PLGC model rats were established by MNNG combined with composite factors, and randomly divided into 6 groups (20 rats/group): the blank group (untreated), model group (treated with normal saline), Weimeisu group (0.05 g/mL Weimeisu), JPFWG low-dose group (JPFWG-L，0.088 g/mL), JPFWG medium-dose group (JPFWG-M，0.176 g/mL) and JPFWG high-dose group (JPFWG-H， 0.351 g/mL). After being treated with Weimeisu and different doses of JPFWG for 12 weeks, the animals were anesthetized and sacrificed, and the gastric tissues were collected. The pathological changes of gastric mucosa were observed by H-E staining, and the expression levels of IL-6-mediated JAK/STAT3 signaling pathway factors (including IL-6, JAK and STAT3) and the mRNA and proteins of their downstream target genes c-Myc and cyclin D1 in gastric mucosal tissues were detected by immunohistochemistry, qPCR and WB. Results: Compared with that in the model group, the gastric mucosal inflammatory cell infiltration was reduced in the Weimeisu group and the low, medium, and high dose groups of JPFWG; pathological condition was improved, most obviously in the high dose group of JPFWG; The protein expressions of IL-6, JAK1 and STAT3 decreased significantly (P < 0.05 or P < 0.01). The expressions of mRNA and proteins of c-Myc and cyclin D1 in the gastric mucosal tissues of the rats in the Weimeisu group and JPFWG-H group decreased significantly (P < 0.05 or P < 0.01). Conclusion: JPFWG can improve the histopathological changes of gastric mucosa in rats with PLGC, and its mechanism may be down-regulating the expressions of c-Myc and cyclin D1 through regulating IL-6/JAK/STAT3 signal pathway, thus blocking inflammation-cancer transformation process.
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