Objective:To investigate the efficacy and mechanism of Jasminoside in dextran sodium sulfate (DSS) -induced ulcerative colitis (UC) mice.Methods:Eighteen C57BL/6 mice were randomly divided into control group, UC group and UC+Jasminoside group, with six mice in each group. The mice in UC group and UC+Jasminoside group freely drank 3%DSS solution for 7 days to induce UC mouse model. The mice in control group freely drank the water without DSS. During the modeling period, the mice in the UC+Jasminoside group were given Jasminoside at a dose of 20 mg/ (kg·d) by gavage for 7 consecutive days, meanwhile the mice in control group and UC group were given equal volumes of distilled water by gavage. The change of body weight and disease activity index (DAI) of the mice were observed daily, and the length of the colon was measured 7 days after the intervention. HE staining was used to observe the inflammatory changes of the colon, and Western blot was used to measure the expression of anti-apoptotic proteins (Bcl-2 and Bcl-xl), caveolin-1 (CAV-1), inducible nitric oxide synthase (iNOS), tight junction proteins (Occludin and Claudin-1). The differences in the above indicators among the mice in three groups were analyzed statistically.Results:All the mice survived. Compared with the control group, the body weight was lower, DAI score was higher, colon was shorter, whose differences were all statistically significant (all P<0.05), and inflammatory infiltration of colon tissue was more severe in mice of UC group. Compared with the UC group, body weight was higher, DAI score was lower, colon was longer, whose differences were all statistically significant (all P<0.05), and inflammatory infiltration of colon tissue was alleviated in mice of UC+Jasminoside group. Western blot results showed that compared with control group, the expression of Bcl-2, Bcl-xl, CAV-1, Occludin and Claudin-1 was significantly lower and the expression of iNOS was significantly higher in the colon tissues of mice in UC group, and the differences were statistically significant (all P<0.05). The expression of Bcl-2, Bcl-xl, CAV-1, Occludin and Claudin-1 in the colon tissues of mice in UC+Jasminoside group was significantly higher than those in UC group, while the expression of iNOS was lower, and the differences were statistically significant (all P<0.05) . Conclusion:Jasminoside can alleviate the symptoms of UC model mice, and its mechanism of action may be related to upregulating the expression of anti-apoptotic proteins and protecting the intestinal mucosal barrier through CAV-1/iNOS pathway.

Objective:To investigate the efficacy and mechanism of Jasminoside in dextran sodium sulfate (DSS) -induced ulcerative colitis (UC) mice.Methods:Eighteen C57BL/6 mice were randomly divided into control group, UC group and UC+Jasminoside group, with six mice in each group. The mice in UC group and UC+Jasminoside group freely drank 3%DSS solution for 7 days to induce UC mouse model. The mice in control group freely drank the water without DSS. During the modeling period, the mice in the UC+Jasminoside group were given Jasminoside at a dose of 20 mg/ (kg·d) by gavage for 7 consecutive days, meanwhile the mice in control group and UC group were given equal volumes of distilled water by gavage. The change of body weight and disease activity index (DAI) of the mice were observed daily, and the length of the colon was measured 7 days after the intervention. HE staining was used to observe the inflammatory changes of the colon, and Western blot was used to measure the expression of anti-apoptotic proteins (Bcl-2 and Bcl-xl), caveolin-1 (CAV-1), inducible nitric oxide synthase (iNOS), tight junction proteins (Occludin and Claudin-1). The differences in the above indicators among the mice in three groups were analyzed statistically.Results:All the mice survived. Compared with the control group, the body weight was lower, DAI score was higher, colon was shorter, whose differences were all statistically significant (all P<0.05), and inflammatory infiltration of colon tissue was more severe in mice of UC group. Compared with the UC group, body weight was higher, DAI score was lower, colon was longer, whose differences were all statistically significant (all P<0.05), and inflammatory infiltration of colon tissue was alleviated in mice of UC+Jasminoside group. Western blot results showed that compared with control group, the expression of Bcl-2, Bcl-xl, CAV-1, Occludin and Claudin-1 was significantly lower and the expression of iNOS was significantly higher in the colon tissues of mice in UC group, and the differences were statistically significant (all P<0.05). The expression of Bcl-2, Bcl-xl, CAV-1, Occludin and Claudin-1 in the colon tissues of mice in UC+Jasminoside group was significantly higher than those in UC group, while the expression of iNOS was lower, and the differences were statistically significant (all P<0.05) . Conclusion:Jasminoside can alleviate the symptoms of UC model mice, and its mechanism of action may be related to upregulating the expression of anti-apoptotic proteins and protecting the intestinal mucosal barrier through CAV-1/iNOS pathway.