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Gardenia Decoction Prevent Intestinal Mucosal Injury by Inhibiting Pro-inflammatory Cytokines and NF-κB Signaling.

ABSTRACT: Gardenia jasminoides Ellis, which belongs to the Rubiaceae family, is a widely used traditional Chinese medicine. Although effect of Gardenia jasminoides Ellis has been widely reported, its anti-inflammatory role in intestinal mucosal injury induced by LPS remains unclear. In the present study, we investigated the effects of decoction extracted from Gardenia jasminoides on the morphology and intestinal antioxidant capacity of duodenum induced by LPS in mice. Further analysis was carried out in the expression of inflammatory and anti-inflammatory cytokines. Nuclear factor-kappa B (NF-κB) was determined by Western blot. Gardenia jasminoides water extract was qualitative analyzed by high-performance liquid chromatography coupled with electro spray ionization quadrupole time-of-flight mass spectrometry. The results showed that Gardenia decoction markedly inhibited the LPS-induced Tumor necrosis factor (TNF)-α, Interleukin (IL)-6, IL-8, and IL-1 production. It was also observed that Gardenia decoction attenuated duodenum histopathology changes in the mouse models. Furthermore, Gardenia decoction inhibited the expression of NF-κB in LPS stimulated mouse duodenum. These results suggest that Gardenia decoction exerts an anti-inflammatory and antioxidant property by up-regulating the activities of the total antioxidant capacity (T-AOC), the total superoxide dismutase (T-SOD), and glutathione peroxidase (GSH-Px). Gardenia decoction is highly effective in inhibiting intestinal mucosal damage and may be a promising potential therapeutic reagent for intestinal mucosal damage treatment.

SUBMITTER: Cui Y

PROVIDER: S-EPMC6447716 | biostudies-other | 2019

REPOSITORIES: biostudies-other

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Gardenia Decoction Prevent Intestinal Mucosal Injury by Inhibiting Pro-inflammatory Cytokines and NF-κB Signaling.

Cui Yizhe Y Wang Qiuju Q Wang Mengzhu M Jia Junfeng J Wu Rui R

Frontiers in pharmacology 20190328

Gardenia jasminoides Ellis, which belongs to the Rubiaceae family, is a widely used traditional Chinese medicine. Although effect of Gardenia jasminoides Ellis has been widely reported, its anti-inflammatory role in intestinal mucosal injury induced by LPS remains unclear. In the present study, we investigated the effects of decoction extracted from Gardenia jasminoides on the morphology and intestinal antioxidant capacity of duodenum induced by LPS in mice. Further analysis ...[more]

PMID: 30983991

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Project description:Intestinal barrier function defects and dysregulation of intestinal immune responses are two key contributory factors in the pathogenesis of ulcerative colitis (UC). Phenazine biosynthesis-like domain-containing protein (PBLD) was recently identified as a tumor suppressor in gastric cancer, hepatocellular carcinoma, and breast cancer; however, its role in UC remains unclear. Therefore, we analyzed colonic tissue samples from patients with UC and constructed specific intestinal epithelial PBLD-deficient (PBLDIEC-/-) mice to investigate the role of this protein in UC pathogenesis. We found that epithelial PBLD was decreased in patients with UC and was correlated with levels of tight junction (TJ) and inflammatory proteins. PBLDIEC-/- mice were more susceptible to dextran sulfate sodium (DSS)- and 2,4,6-trinitrobenzene sulfonic acid-induced colitis compared with wild-type (WT) mice. In DSS-induced colitis, PBLDIEC-/- mice had impaired intestinal barrier function and greater immune cell infiltration in colonic tissue than WT mice. Furthermore, TJ proteins were markedly reduced in PBLDIEC-/- mice compared with WT mice with colitis. Nuclear factor (NF)-κB activation was markedly elevated and resulted in higher expression levels of downstream effectors (C-C motif chemokine ligand 20, interleukin [IL]-1β, IL-6, and tumor necrosis factor [TNF]-α) in colonic epithelial cells isolated from PBLDIEC-/- mice than WT mice with colitis. PBLD overexpression in intestinal epithelial cells (IECs) consistently inhibited TNF-α/interferon-γ-induced intestinal barrier disruption and TNF-α-induced inflammatory responses via the suppression of NF-κB. In addition, IKK inhibition (IKK-16) rescued excessive inflammatory responses induced by TNF-α in PBLD knockdown FHC cells. Co-immunoprecipitation assays showed that PBLD may interact with IKKα and IKKβ, thus inhibiting NF-κB signaling, decreasing inflammatory mediator production, attenuating colonic inflammation, and improving intestinal barrier function. Modulating PBLD expression may provide a novel approach for treatment in patients with UC.

Project description:Ethnopharmacological relevanceIn Traditional Chinese medicine (TCM) theory, ulcerative colitis (UC) is associated with damp-heat, blood stasis, and intestinal vascular ischemia. Kuijieyuan decoction (KD) is a traditional Chinese medicine based on the above theory and used clinically to alleviate UC injury.MethodsThe main components of KD were analyzed by using high-pressure liquid chromatography (HPLC) and confirmed by UPLC-MS/MS. A UC model was established in rats by using dextran sulfate sodium (DSS) and dead rats (caused by DSS) were excluded from the study. Forty-eight rats were divided into 6 groups, health control (CG), UC model (UG), sulfasalazine (SG), low-dose KD (LG), middle-dose KD (MG), and high-dose KD (HG) groups. UC damage was assessed by hematoxylin and eosin staining and scan electron microscopy. We measured Toll-like receptor 4 (TLR4), p-phosphatidylinositol 3-kinase (PI3K), PI3K, p-Protein kinase B (AKT), AKT, p-nuclear factor kappa B (NF-κB), NF-κB, oxidative stress marker (superoxidase dismutase (SOD), catalase (CAT), glutathione peroxidases (GPx), and malondialdehyde) and inflammatory markers (tumor necrosis factor α (TNFα), interleukin (IL)-1, IL-6 and IL-10) in UC tissues. Gut microbiota was analyzed through16S rRNA sequencing.ResultsThe main components of KD consist of gallic acid, paeoniflorin, emodin, berberine, coptisine, palmatine, jatrorrhizine, baicalein and baicalin. The UC model was successfully established by causing intestinal barrier injury with the loss of intestinal villi and destructed mitochondria of intestinal epithelial cells. Both sulfasalazine and KD treatment repaired UC injury, reduced the levels of malondialdehyde, TNFα, IL-1, IL-6, TLR4, p-PI3K, p-AKT, and p-NF-κB, and increased the levels of SOD, GPx, CAT, and IL-10. KD showed a protective function for the UC model in a dose-dependent way. The serum levels of paeoniflorin and baicalin had a strong relationship with the levels of inflammatory and oxidative stress biomarkers. KD treatment increased the proportion of Alloprevotella, Treponema, Prevotellaceae, and Prevotella, and reduced the proportion of Escherichia_Shigella and Desulfovibrio in gut microbiota.ConclusionsKD improved intestinal barrier injury of ulcerative colitis, antioxidant and anti-inflammatory properties by affecting TLR4-dependent PI3K/AKT/NF-κB signaling possibly through the combination of its main compounds, and improving gut microbiota.

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Gardenia Decoction Prevent Intestinal Mucosal Injury by Inhibiting Pro-inflammatory Cytokines and NF-κB Signaling.

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<i>Gardenia</i> Decoction Prevent Intestinal Mucosal Injury by Inhibiting Pro-inflammatory Cytokines and NF-κB Signaling.

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