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The Sasa quelpaertensis Leaf Extract Inhibits the Dextran Sulfate Sodium-induced Mouse Colitis Through Modulation of Antioxidant Enzyme Expression.

Yeom Y, Kim Y - J Cancer Prev (2015)

Bottom Line: Levels of 8-oxo-dG, an oxidative DNA damage marker, were significantly lower in the SQE group compared to the untreated DSS Ctrl group.In the SQE (300 mg/kg) group, MDA levels were significantly lower, while SOD and catalase activity levels in the plasma samples were significantly higher compared with the DSS Ctrl group.The expression levels of the antioxidant enzymes, SOD2 and Gpx1, were significantly higher, while the levels of SOD 1 expression were lower, in the colon tissues of the DSS Ctrl group compared with those of the Ctrl group.

View Article: PubMed Central - PubMed

Affiliation: Department of Nutritional Science and Food Management, College of Health Sciences, Ewha Womans University, Seoul, Korea.

ABSTRACT

Background: Oxidative stress plays an important role in the pathogenesis of inflammatory bowel disease. The objective of this study is to investigate the protective effect of Sasa quelpaertensis leaf extract (SQE) against oxidative stress in mice with dextran sulfate sodium (DSS)-induced colitis.

Methods: Mice were treated with SQE (100 mg/kg or 300 mg/kg body weight) by gavage in advance two weeks before inflammation was induced. Then, the mice were administered with 2.5% DSS in drinking water for 7 days and normal drinking water for 7 days between two DSS treatment. Disease activity index values, gut motility, and severity of the resulting oxidative DNA damage were analyzed. The antioxidant effect of SQE was evaluated by measuring malondialdehyde (MDA) and superoxide dismutase (SOD) activity in plasma samples. Catalase activity and expressions levels of glutathione peroxidase 1 (Gpx1), SOD1, and SOD2 were also detected in colon tissues.

Results: Administration of SQE significantly reduced the severity of DSS-induced colitis compared to the control (Ctrl) group. Levels of 8-oxo-dG, an oxidative DNA damage marker, were significantly lower in the SQE group compared to the untreated DSS Ctrl group. In the SQE (300 mg/kg) group, MDA levels were significantly lower, while SOD and catalase activity levels in the plasma samples were significantly higher compared with the DSS Ctrl group. The expression levels of the antioxidant enzymes, SOD2 and Gpx1, were significantly higher, while the levels of SOD 1 expression were lower, in the colon tissues of the DSS Ctrl group compared with those of the Ctrl group. In contrast, administration of SQE significantly down-regulated SOD2 and Gpx1 expressions and up-regulated SOD1 expression.

Conclusions: These results indicate that SQE efficiently suppresses oxidative stress in DSS-induced colitis in mice, and its action is associated with the regulation of antioxidant enzymes.

No MeSH data available.


Related in: MedlinePlus

Administration of SQE alters gut motility in DSS-induced colitis model. (A) Gut transit time for all groups was analyzed by measuring the time of first development of red stools after carmine red administration. (B) Gut motility was estimated by the time and colon length for each group. Data are shown to as the mean ± SEM and were analyzed using one-way ANOVA and Tukey’s post-hoc test (P < 0.05); n = 10 mice per group. Different letters are used to indicate significant differences. SQE, Sasa quelpaertensis extract; DSS, dextran sulfate sodium; Ctrl, control; SSZ, sulfasalazine.
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f2-jcp-20-136: Administration of SQE alters gut motility in DSS-induced colitis model. (A) Gut transit time for all groups was analyzed by measuring the time of first development of red stools after carmine red administration. (B) Gut motility was estimated by the time and colon length for each group. Data are shown to as the mean ± SEM and were analyzed using one-way ANOVA and Tukey’s post-hoc test (P < 0.05); n = 10 mice per group. Different letters are used to indicate significant differences. SQE, Sasa quelpaertensis extract; DSS, dextran sulfate sodium; Ctrl, control; SSZ, sulfasalazine.

Mentions: To determine the effects of SQE on gut motility, whole gut transit time was measured according to the first appearance of a carmine red stained stool (Fig. 2A). There was no significant difference in gut transit time between the groups although the administration of SQE groups tended to have a shorter time than the Ctrl group. When gut motility was determined by dividing the gut transit time by colon length, gut motility was found to be significantly reduced in the DSS Ctrl group compared to the Ctrl group (Fig. 2B), while gut motility for the SQE groups tended to be increased compared to the DSS Ctrl group. However, the differences were not statistically significant.


The Sasa quelpaertensis Leaf Extract Inhibits the Dextran Sulfate Sodium-induced Mouse Colitis Through Modulation of Antioxidant Enzyme Expression.

Yeom Y, Kim Y - J Cancer Prev (2015)

Administration of SQE alters gut motility in DSS-induced colitis model. (A) Gut transit time for all groups was analyzed by measuring the time of first development of red stools after carmine red administration. (B) Gut motility was estimated by the time and colon length for each group. Data are shown to as the mean ± SEM and were analyzed using one-way ANOVA and Tukey’s post-hoc test (P < 0.05); n = 10 mice per group. Different letters are used to indicate significant differences. SQE, Sasa quelpaertensis extract; DSS, dextran sulfate sodium; Ctrl, control; SSZ, sulfasalazine.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4492358&req=5

f2-jcp-20-136: Administration of SQE alters gut motility in DSS-induced colitis model. (A) Gut transit time for all groups was analyzed by measuring the time of first development of red stools after carmine red administration. (B) Gut motility was estimated by the time and colon length for each group. Data are shown to as the mean ± SEM and were analyzed using one-way ANOVA and Tukey’s post-hoc test (P < 0.05); n = 10 mice per group. Different letters are used to indicate significant differences. SQE, Sasa quelpaertensis extract; DSS, dextran sulfate sodium; Ctrl, control; SSZ, sulfasalazine.
Mentions: To determine the effects of SQE on gut motility, whole gut transit time was measured according to the first appearance of a carmine red stained stool (Fig. 2A). There was no significant difference in gut transit time between the groups although the administration of SQE groups tended to have a shorter time than the Ctrl group. When gut motility was determined by dividing the gut transit time by colon length, gut motility was found to be significantly reduced in the DSS Ctrl group compared to the Ctrl group (Fig. 2B), while gut motility for the SQE groups tended to be increased compared to the DSS Ctrl group. However, the differences were not statistically significant.

Bottom Line: Levels of 8-oxo-dG, an oxidative DNA damage marker, were significantly lower in the SQE group compared to the untreated DSS Ctrl group.In the SQE (300 mg/kg) group, MDA levels were significantly lower, while SOD and catalase activity levels in the plasma samples were significantly higher compared with the DSS Ctrl group.The expression levels of the antioxidant enzymes, SOD2 and Gpx1, were significantly higher, while the levels of SOD 1 expression were lower, in the colon tissues of the DSS Ctrl group compared with those of the Ctrl group.

View Article: PubMed Central - PubMed

Affiliation: Department of Nutritional Science and Food Management, College of Health Sciences, Ewha Womans University, Seoul, Korea.

ABSTRACT

Background: Oxidative stress plays an important role in the pathogenesis of inflammatory bowel disease. The objective of this study is to investigate the protective effect of Sasa quelpaertensis leaf extract (SQE) against oxidative stress in mice with dextran sulfate sodium (DSS)-induced colitis.

Methods: Mice were treated with SQE (100 mg/kg or 300 mg/kg body weight) by gavage in advance two weeks before inflammation was induced. Then, the mice were administered with 2.5% DSS in drinking water for 7 days and normal drinking water for 7 days between two DSS treatment. Disease activity index values, gut motility, and severity of the resulting oxidative DNA damage were analyzed. The antioxidant effect of SQE was evaluated by measuring malondialdehyde (MDA) and superoxide dismutase (SOD) activity in plasma samples. Catalase activity and expressions levels of glutathione peroxidase 1 (Gpx1), SOD1, and SOD2 were also detected in colon tissues.

Results: Administration of SQE significantly reduced the severity of DSS-induced colitis compared to the control (Ctrl) group. Levels of 8-oxo-dG, an oxidative DNA damage marker, were significantly lower in the SQE group compared to the untreated DSS Ctrl group. In the SQE (300 mg/kg) group, MDA levels were significantly lower, while SOD and catalase activity levels in the plasma samples were significantly higher compared with the DSS Ctrl group. The expression levels of the antioxidant enzymes, SOD2 and Gpx1, were significantly higher, while the levels of SOD 1 expression were lower, in the colon tissues of the DSS Ctrl group compared with those of the Ctrl group. In contrast, administration of SQE significantly down-regulated SOD2 and Gpx1 expressions and up-regulated SOD1 expression.

Conclusions: These results indicate that SQE efficiently suppresses oxidative stress in DSS-induced colitis in mice, and its action is associated with the regulation of antioxidant enzymes.

No MeSH data available.


Related in: MedlinePlus