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The Expression of the Mice Intestinal TLR4/NF-κb Signaling Pathway after Short-term High-fat Diet

Author: NaDiLa
Tutor: WangNing
School: Xinjiang Medical University
Course: Internal Medicine
Keywords: TLR4/NF-κB Short-term high-fat diet Intestines Local inflammatoryresponse
CLC: R587.1
Type: Master's thesis
Year: 2012
Downloads: 53
Quote: 0
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Objective: To explore the activation of the mice intestinal TLR4/NF-κB signal pathwaycaused by short-term high-fat diet and the function of the signal pathway in the localenteric inflammatory response. Methods: C57BL/6mice (60) were randomly divided into6high-fat diet groups, feeding for0,1,3,5,7,9days respectively, each group including10mice. The changing of bowel mucosa was observed by HE staining method.Immunohistochemistry was used to detect the expression of inflammation factorsincluding TNF-α, IL-6and describe the formation and development of local intestinalinflammation. Western-blot was used to determine the proteins of TLR4, NF-κB and PIκB.RT-PCR was used to evaluate expression of TLR4mRNA and NF-κB mRNA. Results: Itwas found that there was no obvious pathologic changing in mice intestinal mucosa atdays0,1,3and5, but there were few macrophages diffusing at days7and9by HE.Immunohistochemistry results confirmed that the remaining groups expressed TNF-α andIL-6with increasing frequency except for0day, which had the same activation level asTLR4/NF-κB. Western-blot and RT-PCR tests showed TLR4/NF-κB express in1,3,5,7,and9time groups trending upward and reach a maximum at day7(P<0.05), after whicheach group expressed PIκB and trended downward, and reached minmum in9day(P<0.05). Conclusion: Short-term high-fat diet can cause a local intestinal inflammatoryresponse in mice. There was an activation of TLR4/NF-κB at the initial stage of theinflammation, and the level of activation showed an upward trend correlated with time. Itshowed that TLR4/NF-κB play an important role in the local intestinal inflammatoryresponse caused by short-term high-fat diet and may be the triggering factor.

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