Lianpo Yin Ameliorates Bile Reflux Gastritis in Rats by Regulating TLR4/NF-κB Signaling Pathway
10.13422/j.cnki.syfjx.20260666
- VernacularTitle:基于TLR4/NF-κB信号通路探究连朴饮对胆汁反流性胃炎大鼠的作用机制
- Author:
Yuqing XIE
1
;
Yutian CUI
1
;
Junna ZHANG
2
;
Chunjiang CAI
1
Author Information
1. School of Traditional Chinese Medicine，Hebei University of Chinese Medicine，Shijiazhuang 050091，China
2. Hebei General Hospital，Shijiazhuang 050051，China
- Publication Type:Journal Article
- Keywords:
Lianpo Yin;
bile reflux gastritis;
Toll-like receptor 4/nuclear factor-κB （TLR4/NF-κB） signaling pathway;
inflammatory response;
gastric mucosal injury
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(22):22-30
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the ameliorative effect of Lianpo Yin on gastric mucosal injury in the rat model of bile reflux gastritis （BRG） and decipher the underlying mechanism based on the Toll-like receptor 4 （TLR4）/nuclear factor-κB （NF-κB） signaling pathway. MethodsThirty-six SPF-grade male Sprague-Dawley （SD） rats were randomized into blank， model， hydrotalcite （positive control drug， 0.20 g·kg-1）， NF-κB inhibitor （BAY11-7082， 5.00 mg·kg-1）， low-dose Lianpo Yin （LPY-L， 9.77 g·kg-1）， and high-dose Lianpo Yin （LPY-H， 19.54 g·kg-1） groups （n=6）. Except that the blank group was administrated with distilled water by gavage， the rats in the other groups were induced for the modeling of BRG by gavage with reflux fluid for 35 consecutive days. From the 2nd week of modeling， each treatment group was administrated with the corresponding drugs by gavage 6 h after the end of daily reflux fluid gavage. The BAY11-7082 group received intraperitoneal injection. Meanwhile， the blank group and model group received an equal volume of distilled water by gavage. All interventions were performed for 28 consecutive days. During the experiment period， the general status of rats was observed and body mass changes were recorded， and the stomach index was calculated after the last administration. The histopathological changes of the gastric mucosa were observed under the light microscope after hematoxylin-eosin （HE） staining. The serum levels of tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6） were quantified by enzyme-linked immunosorbent assay （ELISA）. The protein levels of TLR4， NF-κB p65， phosphorylated NF-κB p65 （p-NF-κB p65） and IL-6 in the gastric mucosal tissue were determined by Western blot. The nuclear translocation of NF-κB p65 was observed by immunofluorescence （IF） staining. ResultsCompared with the blank group， the model group showed mental depression， retarded body weight gain （P<0.05， P<0.01）， an increased stomach index （P<0.01）， severely damaged gastric mucosal structure with massive inflammatory cell infiltration and intestinal metaplasia （P<0.01）， elevated serum levels of TNF-α and IL-6 （P<0.01）， up-regulated protein levels of TLR4， p-NF-κB p65/NF-κB p65， and IL-6 in the gastric tissue （P<0.01）， and evident nuclear translocation of NF-κB p65 （P<0.01）. Compared with the model group， all drug intervention groups showed improved general status of rats. The body mass of rats in the hydrotalcite group， LPY-L， and LPY-H groups increased （P<0.05）， while the average body mass of rats in the BAY11-7082 group was slightly higher than that in the model group at each time point. All drug intervention groups showed decreased stomach index （P<0.05， P<0.01）， alleviated pathological damage of gastric mucosa with reduced inflammatory cell infiltration （P<0.05， P<0.01）， and declined serum levels of TNF-α and IL-6 （P<0.01）. Hydrotalcite and LPY-L reduced the levels of TLR4 and IL-6 （P<0.05）， but had no significant effect on p-NF-κB p65. LPY-H down-regulated the protein levels of TLR4， p-NF-κB p65/NF-κB p65， and IL-6 and inhibited the nuclear translocation of NF-κB p65 （P<0.01）， with its effect equivalent to that of BAY11-7082 and superior to that of hydrotalcite and LPY-L. ConclusionLianpo Yin can effectively ameliorate gastric mucosal inflammatory injury in BRG rats by inhibiting the activation of the TLR4/NF-κB signaling pathway， reducing the release of downstream pro-inflammatory cytokines， and suppressing the nuclear translocation of NF-κB p65.
