Limits...
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.


The expression levels of IL-1β and β-actin in the intestine of the mice from each group. (A) Blank control; (B) normal saline; (C) propylene glycol; (D) 0.2 mg/kg triptolide; (E) 0.4 mg/kg triptolide; (F) 0.6 mg/kg triptolide; and (G) dexamethasone treatment groups. The ratio of IL-1β protein to β-actin as determined by densitometry is shown. The data are presented as the mean ± standard deviation. *P<0.01, vs. the expression levels in the propylene glycol and normal saline treatment groups. IL, interleukin.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4997980&req=5

f4-etm-0-0-3490: The expression levels of IL-1β and β-actin in the intestine of the mice from each group. (A) Blank control; (B) normal saline; (C) propylene glycol; (D) 0.2 mg/kg triptolide; (E) 0.4 mg/kg triptolide; (F) 0.6 mg/kg triptolide; and (G) dexamethasone treatment groups. The ratio of IL-1β protein to β-actin as determined by densitometry is shown. The data are presented as the mean ± standard deviation. *P<0.01, vs. the expression levels in the propylene glycol and normal saline treatment groups. IL, interleukin.

Mentions: IL-1β protein expression was detected by western blot analysis. Fig. 4 shows the western blot images of IL-1β and β-actin in each group. As compared with the weak IL-1β protein expression levels detected in the colonic mucosa tissue of mice in the blank control group, IL-1β protein expression levels were significantly upregulated in the normal saline and propylene glycol treatment groups (P<0.01). Furthermore, as compared with the blank control group, IL-1β protein expression levels were markedly increased in the TL2, TL3 and dexamethasone treatment groups, and were significantly decreased, as compared with the normal saline and propylene glycol treatment groups (P<0.01). No significant differences were detected among the TL2, TL3 and dexamethasone treatment groups. The results suggest that treatment with TL and dexamethasone may suppress IL-1β expression in colon tissue.


Therapeutic effects of triptolide via the inhibition of IL-1 β expression in a mouse model of ulcerative colitis
The expression levels of IL-1β and β-actin in the intestine of the mice from each group. (A) Blank control; (B) normal saline; (C) propylene glycol; (D) 0.2 mg/kg triptolide; (E) 0.4 mg/kg triptolide; (F) 0.6 mg/kg triptolide; and (G) dexamethasone treatment groups. The ratio of IL-1β protein to β-actin as determined by densitometry is shown. The data are presented as the mean ± standard deviation. *P<0.01, vs. the expression levels in the propylene glycol and normal saline treatment groups. IL, interleukin.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f4-etm-0-0-3490: The expression levels of IL-1β and β-actin in the intestine of the mice from each group. (A) Blank control; (B) normal saline; (C) propylene glycol; (D) 0.2 mg/kg triptolide; (E) 0.4 mg/kg triptolide; (F) 0.6 mg/kg triptolide; and (G) dexamethasone treatment groups. The ratio of IL-1β protein to β-actin as determined by densitometry is shown. The data are presented as the mean ± standard deviation. *P<0.01, vs. the expression levels in the propylene glycol and normal saline treatment groups. IL, interleukin.
Mentions: IL-1β protein expression was detected by western blot analysis. Fig. 4 shows the western blot images of IL-1β and β-actin in each group. As compared with the weak IL-1β protein expression levels detected in the colonic mucosa tissue of mice in the blank control group, IL-1β protein expression levels were significantly upregulated in the normal saline and propylene glycol treatment groups (P<0.01). Furthermore, as compared with the blank control group, IL-1β protein expression levels were markedly increased in the TL2, TL3 and dexamethasone treatment groups, and were significantly decreased, as compared with the normal saline and propylene glycol treatment groups (P<0.01). No significant differences were detected among the TL2, TL3 and dexamethasone treatment groups. The results suggest that treatment with TL and dexamethasone may suppress IL-1β expression in colon tissue.

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.