LI Chen, YU Yuan, FAN Yao-fu, et al. Effect of Shaohuang Anchang Decoction on TLR4/Myd88/NF-B Signaling Pathway in Ulcerative Colitis Rats[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(7): 151-155.
DOI:
LI Chen, YU Yuan, FAN Yao-fu, et al. Effect of Shaohuang Anchang Decoction on TLR4/Myd88/NF-B Signaling Pathway in Ulcerative Colitis Rats[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(7): 151-155. DOI: 10.13422/j.cnki.syfix.2014070151.
Effect of Shaohuang Anchang Decoction on TLR4/Myd88/NF-B Signaling Pathway in Ulcerative Colitis Rats
Objective: To observe the effect of Shaohuang Anchang decoction (SAD) on Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-κB(NF-κB) in colonic mucosa of rats with ulcerative colitis(UC)
and to explore its possible mechanism. Method: The rat UC model was induced by trinitro-benzene-sulfonic acid (TNBS)/anhydrous alcohol.The SD rats were randomized into the normal group
model group
SAD low-dose group
SAD middle-dose group
SAD high-dose group (4.5
9
18 g·kg-1)and the Mesalazine group(5 g·kg-1)
with 10 in each. Since the 2nd day of modeling
corresponding medications were respectively administered to each treatment group by gastrogavage for 10 successive days.Disease activity index (DAI)
colon macroscopic damage score (CMDS) were calculated
The expression of NF-κB in the colonic mucosa was detected by immunohistochemistry.The expressions of TLR4 mRNA and MyD88 mRNA were detected with reverse transcription-polymerase chain reaction. Result: Compared with the normal group
the model group showed significantly increased DAI
CMDS
but the SAD groups showed more lower than the model group. Compared with the normal group
the expressions of NF-κB
TLR4 mRNA
MyD88 mRNA were significantly increased in other groups. Comparing with the control group
the expressions of NF-κB
TLR4 mRNA
MyD88 mRNA were significantly decreased in the SAD low-dose
middle-dose
high-dose groups and the Mesalazine group
especially in the SAD high-dose group. Conclusion: Treatment with DG could reduce inflammatory injury in rats with ulcerative colitis. Its possible mechanism may be through inhibiting the expression of TLR4 and then inhibiting the activation of MyD88 and NF-κB
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