Abstract:

Objective The aim of this study was to investigate whether the mechanism of high⁃salt diet in intestinal barrier function was related with the activation of the signaling pathway of Janus kinase 1⁃signal transducer and activator of transcription 3（JAK1⁃STAT3）. Methods SPF C57BL/6 mice weighing（20 ± 5）g were randomly divided into control group and high salt diet（HSD）group. There were 5 mice in each group. Control group was fed with standard chow ad libitum，while the high⁃salt diet was achieved by feeding a dietary chow consisting of 8% NaCl for 12 weeks. At the end of feeding，the intestinal tissue samples were collected to analyze the intestinal barrier function and the activity JAK1⁃STAT3 signaling pathway. Human normal colon epithelial cell line NCM ⁃ 460 was used for cell experiments：（1）Control group（Control）；（2）High salt treatment group（High NaCl，50 mmol/L） for 48 h；3）JAK1 inhibitor Ruxolitinib treatment group（High NaCl + Ruxolitinib），pretreatment with JAK1 inhibi⁃ tor Ruxolitinib（50 μmol/L）for 2 hours，then add high concentration NaCl（50 mmol/L）and incubate for 46 hours. After the cells were processed，the cells were collected to detect the intestinal epithelial barrier tight junc⁃ tion proteins and the changes of JAK1⁃STAT3 signaling pathway proteins by Western blot. Results High⁃salt diet could inhibit the expression of intestinal barrier protein and increase the permeability of intestinal barrier as well as activate the expression of JAK1⁃STAT3 signaling pathway protein in the intestinal tissue. JAK1 inhibitor Ruxolitinib resisted intestinal barrier dysfunction induced by high concentration of NaCl. Conclusion High ⁃salt diet may induce intestinal barrier dysfunction by activating JAK

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