PROTECTIVE EFFECT OF SODIUM BUTYRATE ON INTESTINAL BARRIER IN HYPERURICEMIA MOUSE MODEL

Abstract

Objective To investigate the protective effect of sodium butyrate on intestinal barrier in mice with hyperuricemia. Methods Male C57BL/6 mice were randomly divided into control group, model group, and sodium butyrate group. Mice in the model group were intraperitoneally injected with potassium oxonate (250 mg/kg) every day, and fed with high yeast diet freely. Mice in the sodium butyrate group were given 200 mg/kg sodium butyrate by gavage every day on the basis of the treatment in the model group. Mice in the control group were intraperitoneally injected and intragastrically administered with the same dose of normal saline every day. The intervention lasted for 21 d. The expression levels of ZO-1 and Occludin protein and mRNA in small intestine tissues of mice in each group were measured by Western blot, real-time quantitative polymerase chain reaction (RT-qPCR), and immunohistochemical staining. The pathological morphology of small intestine tissues in each group was observed by hematoxylin-eosin (HE) staining. The content of inflammatory factors in small intestine tissues was measured by enzyme-linked immunosorbent assay (ELISA). Results There was a significant difference in body mass among the three groups (F=4.70,P<0.05). The body mass of the model group was significantly lower than that of the control group (t=3.03,P<0.05), and the body mass of the sodium butyrate group was significantly higher than that of the model group (t=2.90,P<0.05). The results of Western blot, RT-qPCR, and immunohistochemical staining showed that there were significant differences in the expression of ZO-1 and Occludin protein and mRNA in the small intestine between the model group and the control group, the model group and the sodium butyrate group (t=2.55-11.04,P<0.05). The results of HE staining showed that the small intestinal villi of the mo-del group were significantly reduced and broken, and the small intestinal villi of the sodium butyrate group were relatively complete. ELISA results showed that there were significant differences in the levels of tumor necrosis factor-α and interleukin-6 in the small intestine between the model group and the control group, the model group and the sodium butyrate group (t=5.74-9.79,P<0.05). Conclusion Hyperuricemia mouse models have intestinal barrier injury, and intragastric administration of sodium butyrate can protect the intestinal barrier of hyperuricemia model mice.

Keywords

• hyperuricemia|intestines|osmosis|butyric acid|tight junction proteins|disease models, animal|mice