Exprossion of TLR4 and NF-κB in rats model induced with IBS-D and its mechanism
10.11855/j.issn.0577-7402.2019.08.04
- Author:
Lu-Lu BAO
1
Author Information
1. Naval Clinical College, Anhui Medical University
- Publication Type:Journal Article
- Keywords:
Diarrhea-predominant irritable bowel syndrome;
Inflammatory factor;
Rats
- From:
Medical Journal of Chinese People's Liberation Army
2019;44(8):648-651
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To analyze the dynamic changes of inflammatory factors in rats model induced with IBS-D. Methods: Thirty Wistar rats were randomly divided into the blank group, the IBS-D group, and the TAK-242 group. All rats received acute and chronic stress method, followed by no further treatment for the blank group. To induce IBS-D, before performing acute and chronic stress, the IBS-D group received 3 mg/kg saline. To explore the potential mechanism of TLR4 in IBS-D, TAK-242, an antagonist of TLR4 was given to 3 mg/kg TAK-242 group after they received acute and chronic stress. Fecal traits were evaluated by Bristol classification at 0, 7, 14, 21, 28 days, and the levels of MyD88, IL-1β, IL-6 were quantified by Elisa assays; and the levels of TLR4, NF-κB were detected by Western blot. Results: In the blank group, there was no significant change in the scores of Bristol stool and expression levels of MyD88, IL-1β, IL-6, TLR4 and NF-κB at the 7th, 14th, 21st and 28th day. Compared with the blank group, in the IBS-D rats and TAK-242 rats, the scores of Bristolian stools (P<0.05), the levels of MyD88 and serum inflammatory factors (P<0.05), TLR4, NF-κB were all increased (P<0.05). However, the scores of Bristolian stools and the expression levels of MyD88, IL-1β, IL-6, TLR4, and NF-κB in the TAK-242 group were lower than those in the IBS-D group, suggesting therapeutic effects of TAK-242 in IBS-D. Conclusions: IBS-D may increase inflammatory factors through activating the TLR4/MyD88/NF-κB signaling pathway, resulting in disease progression.
