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Rabeprazole destroyed gastric epithelial barrier function through FOXF1/STAT3-mediated ZO-1 expression.

Fangying Yang¹, Linkai Li², Yanhe Zhou¹

¹Department of Gastroenterology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.

Clinical and Experimental Pharmacology & Physiology

|March 10, 2023

Summary

Rabeprazole reduces ZO-1 expression, impairing gut barrier function by inhibiting the FOXF1/STAT3 pathway. This study reveals a novel mechanism impacting gastric epithelial cells, necessitating treatment evaluation.

Keywords:

FOXF1 STAT3 ZO-1 barrier function rabeprazole

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Area of Science:

Gastroenterology
Molecular Biology
Cell Biology

Background:

Proton pump inhibitors like Rabeprazole are widely used for anti-ulcer treatment.
The impact of Rabeprazole on gut barrier function is not fully understood.

Purpose of the Study:

To investigate the effect of Rabeprazole on gut barrier function.
To elucidate the underlying molecular mechanism involving ZO-1 expression and the FOXF1/STAT3 pathway.

Main Methods:

Immunofluorescence (IF) analysis to assess ZO-1 expression.
Western blotting (WB) and real-time PCR (qPCR) to quantify gene and protein expression.
Investigated phosphorylation, nuclear translocation, and protein-protein interactions of FOXF1 and STAT3.

Main Results:

Rabeprazole treatment significantly decreased ZO-1 expression in gastric epithelial cells.
Rabeprazole inhibited the FOXF1/STAT3 pathway by reducing phosphorylation of STAT3 and FOXF1.
This inhibition led to decreased nuclear translocation and binding of STAT3/FOXF1 to the ZO-1 promoter, disrupting barrier function.

Conclusions:

Rabeprazole impairs gastric epithelial barrier function through the novel Rabeprazole/FOXF1/STAT3/ZO-1 pathway.
Overexpression of STAT3 and FOXF1 can reverse Rabeprazole's inhibitory effects on ZO-1.
Findings suggest a need for comprehensive consideration in Rabeprazole treatment regimens.