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2016 ; 12
(3
): 1279-1286
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Therapeutic effects of triptolide via the inhibition of IL-1? expression in a
mouse model of ulcerative colitis
#MMPMID27588050
Zhang H
; Gong C
; Qu L
; Ding X
; Cao W
; Chen H
; Zhang B
; Zhou G
Exp Ther Med
2016[Sep]; 12
(3
): 1279-1286
PMID27588050
show ga
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? 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? were evaluated by enzyme-linked immunosorbent
assay, and IL-1? 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? 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-1?
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-1? expression was upregulated in the UC
mouse model, which may be associated with the development and progression of UC.
Furthermore, TL inhibited IL-1? expression, suggesting that TL may be a novel
therapeutic target for the treatment of UC.