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Flavonoids Extracted from Licorice Prevents Colitis-Associated Carcinogenesis in AOM/DSS Mouse Model

View Article: PubMed Central - PubMed

ABSTRACT

Inflammatory bowel disease (IBD) is generally considered as a major risk factor in the progression of colitis-associated carcinogenesis (CAC). Thus, it is well accepted that ameliorating inflammation creates a potential to achieve an inhibitory effect on CAC. Licorice flavonoids (LFs) possess strong anti-inflammatory activity, making it possible to investigate its pharmacologic role in suppressing CAC. The purpose of the present study was to evaluate the anti-tumor potential of LFs, and further explore the underlying mechanisms. Firstly, an azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced mouse model was established and administered with or without LFs for 10 weeks, and then the severity of CAC was examined macroscopically and histologically. Subsequently, the effects of LFs on expression of proteins associated with apoptosis and proliferation, levels of inflammatory cytokine, expression of phosphorylated-Janus kinases 2 (p-Jak2) and phosphorylated-signal transducer and activator of transcription 3 (p-Stat3), and activation of nuclear factor-κB (NFκB) and P53 were assessed. We found that LFs could significantly reduce tumorigenesis induced by AOM/DSS. Further study revealed that LFs treatment substantially reduced activation of NFκB and P53, and subsequently suppressed production of inflammatory cytokines and phosphorylation of Jak2 and Stat3 in AOM/DSS-induced mice. Taken together, LFs treatment alleviated AOM/DSS induced CAC via P53 and NFκB/IL-6/Jak2/Stat3 pathways, highlighting the potential of LFs in preventing CAC.

No MeSH data available.


Related in: MedlinePlus

Effects of LFs on colitis-associated colon carcinogenesis were evaluated in C57BL/6 mice. (A) Schematic of administration of AOM, DSS and LFs to mice. Fifteen mice were set in the model control group, and 10 mice per group were set in other groups; (B) Effect of LFs on the body weight of mice. During experiment, mice were weighed once a week for 10 weeks; (C) Effect of LFs on the survival rate of mice. LFs prolonged animal survival. Data are presented as mean vs. control and model.
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ijms-17-01343-f001: Effects of LFs on colitis-associated colon carcinogenesis were evaluated in C57BL/6 mice. (A) Schematic of administration of AOM, DSS and LFs to mice. Fifteen mice were set in the model control group, and 10 mice per group were set in other groups; (B) Effect of LFs on the body weight of mice. During experiment, mice were weighed once a week for 10 weeks; (C) Effect of LFs on the survival rate of mice. LFs prolonged animal survival. Data are presented as mean vs. control and model.

Mentions: To examine the effect of LFs on CAC, mutagen AOM was used to initiate colon tumors, followed by repeated DSS administration to induce chronic inflammation (Figure 1A). Mice receiving vehicle alone were used as a control group. Throughout the AOM/DSS treatment, mice were orally administrated with LFs (0, 50, and 100 mg/kg) once a day for 10 weeks. As shown in Figure 1B, significant body weight loss was observed in AOM/DSS induced mice when compared with the control group, which appeared to be alleviated by LFs treatment but this was not significant. Moreover, the survival rate of AOM/DSS induced mice was significantly increased after LFs treatment (50 and 100 mg/kg) based on Kaplan–Meier survival curves (Figure 1C), with survival rates of 66% and 80% at the end of the experiment, respectively.


Flavonoids Extracted from Licorice Prevents Colitis-Associated Carcinogenesis in AOM/DSS Mouse Model
Effects of LFs on colitis-associated colon carcinogenesis were evaluated in C57BL/6 mice. (A) Schematic of administration of AOM, DSS and LFs to mice. Fifteen mice were set in the model control group, and 10 mice per group were set in other groups; (B) Effect of LFs on the body weight of mice. During experiment, mice were weighed once a week for 10 weeks; (C) Effect of LFs on the survival rate of mice. LFs prolonged animal survival. Data are presented as mean vs. control and model.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5037654&req=5

ijms-17-01343-f001: Effects of LFs on colitis-associated colon carcinogenesis were evaluated in C57BL/6 mice. (A) Schematic of administration of AOM, DSS and LFs to mice. Fifteen mice were set in the model control group, and 10 mice per group were set in other groups; (B) Effect of LFs on the body weight of mice. During experiment, mice were weighed once a week for 10 weeks; (C) Effect of LFs on the survival rate of mice. LFs prolonged animal survival. Data are presented as mean vs. control and model.
Mentions: To examine the effect of LFs on CAC, mutagen AOM was used to initiate colon tumors, followed by repeated DSS administration to induce chronic inflammation (Figure 1A). Mice receiving vehicle alone were used as a control group. Throughout the AOM/DSS treatment, mice were orally administrated with LFs (0, 50, and 100 mg/kg) once a day for 10 weeks. As shown in Figure 1B, significant body weight loss was observed in AOM/DSS induced mice when compared with the control group, which appeared to be alleviated by LFs treatment but this was not significant. Moreover, the survival rate of AOM/DSS induced mice was significantly increased after LFs treatment (50 and 100 mg/kg) based on Kaplan–Meier survival curves (Figure 1C), with survival rates of 66% and 80% at the end of the experiment, respectively.

View Article: PubMed Central - PubMed

ABSTRACT

Inflammatory bowel disease (IBD) is generally considered as a major risk factor in the progression of colitis-associated carcinogenesis (CAC). Thus, it is well accepted that ameliorating inflammation creates a potential to achieve an inhibitory effect on CAC. Licorice flavonoids (LFs) possess strong anti-inflammatory activity, making it possible to investigate its pharmacologic role in suppressing CAC. The purpose of the present study was to evaluate the anti-tumor potential of LFs, and further explore the underlying mechanisms. Firstly, an azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced mouse model was established and administered with or without LFs for 10 weeks, and then the severity of CAC was examined macroscopically and histologically. Subsequently, the effects of LFs on expression of proteins associated with apoptosis and proliferation, levels of inflammatory cytokine, expression of phosphorylated-Janus kinases 2 (p-Jak2) and phosphorylated-signal transducer and activator of transcription 3 (p-Stat3), and activation of nuclear factor-κB (NFκB) and P53 were assessed. We found that LFs could significantly reduce tumorigenesis induced by AOM/DSS. Further study revealed that LFs treatment substantially reduced activation of NFκB and P53, and subsequently suppressed production of inflammatory cytokines and phosphorylation of Jak2 and Stat3 in AOM/DSS-induced mice. Taken together, LFs treatment alleviated AOM/DSS induced CAC via P53 and NFκB/IL-6/Jak2/Stat3 pathways, highlighting the potential of LFs in preventing CAC.

No MeSH data available.


Related in: MedlinePlus