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Therapeutic effects of triptolide via the inhibition of IL-1 β expression in a mouse model of ulcerative colitis

View Article: PubMed Central - PubMed

ABSTRACT

The present study aimed to investigate the effect of triptolide (TL) on ulcerative colitis (UC) and explore the potential association between the therapeutic effects of TL and IL-1β expression using a 4,4-dimethyl-4-silapentane-1-sulfonic acid (DSS)-induced mouse model to simulate human UC. A total of 70 BALB/c female mice were randomly allocated into seven equal groups: Group A, blank control; group B, normal saline injection; group C, propylene glycol injection; group D (TL1), 0.2 mg/kg TL; group E (TL2), 0.4 mg/kg TL; group F (TL3), 0.6 mg/kg TL; and group G, dexamethasone injection. Mice activity, diet and stool characteristics were recorded daily. Mice were sacrificed by cervical dislocation on day 8, and disease activity indices, colon tissue histological scores and colonic histopathological scores were subsequently calculated. Serum levels of IL-1β were evaluated by enzyme-linked immunosorbent assay, and IL-1β expression levels were examined by reverse transcription-quantitative polymerase chain reaction with colonic mucosa specimen at the gene level and western blot analysis at the protein level. The IL-1β mRNA and protein expression levels were significantly elevated in the normal saline injection and propylene glycol injection groups compared with the blank control group and (P<0.01). In TL (TL2 and TL3)- and dexamethasone-treated mice, IL-1β expression levels were significantly decreased, as compared with the normal saline and propylene glycol injection groups (P<0.05). No significant difference was detected between TL (TL2 and TL3) and dexamethasone treatments. The results of the present study indicated that IL-1β expression was upregulated in the UC mouse model, which may be associated with the development and progression of UC. Furthermore, TL inhibited IL-1β expression, suggesting that TL may be a novel therapeutic target for the treatment of UC.

No MeSH data available.


DAI scores among the groups from the first day of dosing. DAI, disease activity index; TL, triptolide. *P<0.05, vs. the propylene glycol treatment and normal saline treatment groups.
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f1-etm-0-0-3490: DAI scores among the groups from the first day of dosing. DAI, disease activity index; TL, triptolide. *P<0.05, vs. the propylene glycol treatment and normal saline treatment groups.

Mentions: Characteristics including vigor, body weight, activity, hair color, diet, stool property and hematochezia were assessed from the first day of DSS induction and DAI scores were calculated to assess the effect of TL on UC. Mice in the blank control group exhibited shiny hair, increased body weight, normal vigor and activity levels, and their diet and stool were normal. From the second or third day of receiving normal saline or propylene glycol injection, DSS-induced mice were anorexic, with decreased activity, piloerection, darkened hair color, weight loss and altered stool properties, including loose and soft stools. Hematochezia or occult fecal blood were observed on the fourth day following treatment, accompanies by prominent body weight loss and reduced activity. One mouse in the normal saline group succumbed to the treatment after six days. Mice in the TL2, TL3 and dexamethasone treatment groups exhibited improved diet and body weight, as compared with the normal saline or propylene glycol treatment groups. In addition, the vigor and activity of mice were improved, hair shine and color returned, stool properties returned to normal and hematochezia and occult fecal blood were alleviated (Fig. 1). In summary, The DAI scores of the normal saline injection and propylene glycol injection groups were significantly elevated as compared with the blank control group (P<0.05); conversely, the scores for the TL and dexamethasone treatment groups were significantly decreased (P<0.05). The results suggest that treatment with TL and dexamethasone may alleviate the symptoms of mouse colon ulcerative colitis.


Therapeutic effects of triptolide via the inhibition of IL-1 β expression in a mouse model of ulcerative colitis
DAI scores among the groups from the first day of dosing. DAI, disease activity index; TL, triptolide. *P<0.05, vs. the propylene glycol treatment and normal saline treatment groups.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4997980&req=5

f1-etm-0-0-3490: DAI scores among the groups from the first day of dosing. DAI, disease activity index; TL, triptolide. *P<0.05, vs. the propylene glycol treatment and normal saline treatment groups.
Mentions: Characteristics including vigor, body weight, activity, hair color, diet, stool property and hematochezia were assessed from the first day of DSS induction and DAI scores were calculated to assess the effect of TL on UC. Mice in the blank control group exhibited shiny hair, increased body weight, normal vigor and activity levels, and their diet and stool were normal. From the second or third day of receiving normal saline or propylene glycol injection, DSS-induced mice were anorexic, with decreased activity, piloerection, darkened hair color, weight loss and altered stool properties, including loose and soft stools. Hematochezia or occult fecal blood were observed on the fourth day following treatment, accompanies by prominent body weight loss and reduced activity. One mouse in the normal saline group succumbed to the treatment after six days. Mice in the TL2, TL3 and dexamethasone treatment groups exhibited improved diet and body weight, as compared with the normal saline or propylene glycol treatment groups. In addition, the vigor and activity of mice were improved, hair shine and color returned, stool properties returned to normal and hematochezia and occult fecal blood were alleviated (Fig. 1). In summary, The DAI scores of the normal saline injection and propylene glycol injection groups were significantly elevated as compared with the blank control group (P<0.05); conversely, the scores for the TL and dexamethasone treatment groups were significantly decreased (P<0.05). The results suggest that treatment with TL and dexamethasone may alleviate the symptoms of mouse colon ulcerative colitis.

View Article: PubMed Central - PubMed

ABSTRACT

The present study aimed to investigate the effect of triptolide (TL) on ulcerative colitis (UC) and explore the potential association between the therapeutic effects of TL and IL-1&beta; expression using a 4,4-dimethyl-4-silapentane-1-sulfonic acid (DSS)-induced mouse model to simulate human UC. A total of 70 BALB/c female mice were randomly allocated into seven equal groups: Group A, blank control; group B, normal saline injection; group C, propylene glycol injection; group D (TL1), 0.2 mg/kg TL; group E (TL2), 0.4 mg/kg TL; group F (TL3), 0.6 mg/kg TL; and group G, dexamethasone injection. Mice activity, diet and stool characteristics were recorded daily. Mice were sacrificed by cervical dislocation on day 8, and disease activity indices, colon tissue histological scores and colonic histopathological scores were subsequently calculated. Serum levels of IL-1&beta; were evaluated by enzyme-linked immunosorbent assay, and IL-1&beta; expression levels were examined by reverse transcription-quantitative polymerase chain reaction with colonic mucosa specimen at the gene level and western blot analysis at the protein level. The IL-1&beta; mRNA and protein expression levels were significantly elevated in the normal saline injection and propylene glycol injection groups compared with the blank control group and (P&lt;0.01). In TL (TL2 and TL3)- and dexamethasone-treated mice, IL-1&beta; expression levels were significantly decreased, as compared with the normal saline and propylene glycol injection groups (P&lt;0.05). No significant difference was detected between TL (TL2 and TL3) and dexamethasone treatments. The results of the present study indicated that IL-1&beta; expression was upregulated in the UC mouse model, which may be associated with the development and progression of UC. Furthermore, TL inhibited IL-1&beta; expression, suggesting that TL may be a novel therapeutic target for the treatment of UC.

No MeSH data available.