L-theanine attenuates porcine intestinal tight junction damage induced by LPS via p38 MAPK/NLRP3 signaling in IPEC-J2 cells

Chen, Xiaoling; Luo, Diaoyun; Jia, Gang; Zhao, Hua; Liu, Guangmang; Huang, Zhiqing

doi:10.1016/j.fct.2023.113870

Cited by 9 publications

(3 citation statements)

References 27 publications

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“…Therefore, the intestinal barrier's function plays a central role in the onset and progression of UC [29]. The intestinal epithelial barrier serves as the initial layer of defense against various kinds of bacterial infection and is responsible for maintaining intestinal mucosal homeostasis [30]. The dysfunction of the intestinal epithelial barrier provides growing evidence that increases in intestinal permeability play a pathogenic role in diseases such as IBD [7,28].…”

Section: Discussionmentioning

confidence: 99%

Ziziphus jujuba Miller Ethanol Extract Restores Disrupted Intestinal Barrier Function via Tight Junction Recovery and Reduces Inflammation

Yang,

Kim,

Lee

et al. 2024

Antioxidants

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Inflammatory bowel disease (IBD) is a chronic inflammatory condition caused by the disruption of the intestinal barrier. The intestinal barrier is maintained by tight junctions (TJs), which sustain intestinal homeostasis and prevent pathogens from entering the microbiome and mucosal tissues. Ziziphus jujuba Miller (Z. jujuba) is a natural substance that has been used in traditional medicine as a therapy for a variety of diseases. However, in IBD, the efficacy of Z. jujuba is unknown. Therefore, we evaluated ZJB in Caco2 cells and a dextran sodium sulfate (DSS)-induced mouse model to demonstrate its efficacy in IBD. Z. jujuba extracts were prepared using 70% ethanol and were named ZJB. ZJB was found to be non-cytotoxic and to have excellent antioxidant effects. We confirmed its anti-inflammatory properties via the down-regulation of inflammatory factors, including inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). To evaluate the effects of ZJB on intestinal barrier function and TJ improvement, the trans-epithelial electrical resistance (TEER) and fluorescein isothiocyanate-dextran 4 kDa (FITC-Dextran 4) permeability were assessed. The TEER value increased by 61.389% and permeability decreased by 27.348% in the 200 μg/mL ZJB group compared with the 50 ng/mL IL-6 group after 24 h. Additionally, ZJB alleviated body weight loss, reduced the disease activity index (DAI) score, and induced colon shortening in 5% DSS-induced mice; inflammatory cytokines, tumor necrosis factor (TNF)-α, and interleukin (IL)-6 were down-regulated in the serum. TJ proteins, such as Zonula occludens (ZO)-1 and occludin, were up-regulated by ZJB in an impaired Caco2 mouse model. Additionally, according to the liquid chromatography results, in tandem with mass spectrometry (LC-MS/MS) analysis, seven active ingredients were detected in ZJB. In conclusion, ZJB down-regulated inflammatory factors, protected intestinal barrier function, and increased TJ proteins. It is thus a safe, natural substance with the potential to be used as a therapeutic agent in IBD treatment.

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Section: Discussionmentioning

confidence: 99%

Ziziphus jujuba Miller Ethanol Extract Restores Disrupted Intestinal Barrier Function via Tight Junction Recovery and Reduces Inflammation

Yang,

Kim,

Lee

et al. 2024

Antioxidants

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“…Protein kinases of the MAPK family, including JNK, ERK, and p38, accelerate inflammatory reactions and the release of inflammatory factors. Chen et al have investigated the potential protective effects of L -theanine against intestinal TJ damage ignited by LPS through the p38 MAPK/NLRP3 pathway. Similarly, Zhao et al also pointed out that Ganoderma lucidum spore powder could ameliorate colon inflammation and gut barrier dysfunction by inhibiting the MAPK pathway.…”

Section: Introductionmentioning

confidence: 99%

Galangin Prevents Against Ethanol-Induced Intestinal Barrier Dysfunction and NLRP3 Inflammasome Activation via NF-κB/MAPK Signaling Pathways in Mice and Caco-2 Cells

Zhao,

Li,

Liu

et al. 2024

J. Agric. Food Chem.

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The potential of natural phytochemicals in addressing ethanol-related public safety concerns has been garnering attention. Galangin, a potent flavonoid renowned for its antioxidative and anti-inflammatory characteristics, is derived from the galanga plant, and propolis is derived from bees. Here, we documented the effects of galangin on ethanol-stimulated intestinal tight junction damage and investigated its potential protective mechanism in both in vivo and in vitro models, which has not been extensively investigated. Our results revealed that galangin efficaciously mitigated ethanol-induced intestine injury and dysfunction of the intestinal barrier. Concurrently, galangin significantly counteracted the ethanol-induced upregulation of NLRP3 inflammasomeassociated proteins and activated the mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-κB) signaling pathways in both the mouse colon and Caco-2 cells. Interestingly, similar to galangin, inhibitors of MAPKs and the NF-κB p65 reduced ethanol-induced NLRP3 inflammasome activation and intestinal tight junction damage. To sum up, our results showed that galangin blocks the ethanol-induced perturbation of the intestinal barrier and activation of the NLRP3 inflammasome via the NF-κB/MAPK signaling pathways.

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“…Inhibition of the NLRP3 inflammasome pathway activation protects against LPSinduced intestinal TJ injury and restores the expression of Zonula occludens-1 (ZO-1), Occludin, and Claudin-1 gene [15] . Additionally, several studies have indicated that the family of PARs, including PAR1, PAR2, and PAR4, can activate NLRP3 inflammatory vesicle signaling [16][17][18][19] .…”

Section: Introductionmentioning

confidence: 99%

Trypsin activates PAR2 inhibits the expression of tight junction protein through activation of NLRP3 inflammasome pathway in gastroesophageal reflux disease

Du,

Wang,

Wang

et al. 2023

Preprint

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BACKGROUND: Trypsin activates protease-activated receptor 2 (PAR2), which mediates the initiation of mucosal inflammation in gastroesophageal reflux disease (GERD). Nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome is crucial for the activation of pyroptosis, and inflammation becomes more severe. This study aimed to investigate the effects of PAR2 and NLRP3 on the tight junction (TJ) in the pathogenesis of GERD and the therapeutic effects of rabeprazole. Methods: We constructed a rat GERD model using cardia myotomy and pyloric ligation. Two weeks following rabeprazole administration, we assessed the esophageal mucosal barrier using western blot and immunohistochemistry for Claudin-1 and Claudin-4, while exploring the expression of PAR2, NLRP3, and Caspase-1. Human esophageal epithelial cells (HEECs) were produced with overexpression of PAR2 and treated with PAR2 agonist and inhibitor, respectively, to observe the changes in the NLRP3 pathway and esophageal TJ protein. RESULTS: The expression of Claudin-1 and Claudin-4 decreased, whereas the expression of PAR2, NLRP3, and Caspase-1 increased in the GERD group compared to the Sham group. PAR2 inhibitor reversed these processes. In HEECs, trypsin activated PAR2 and NLRP3 and disrupted TJ protein. PAR2 agonist played an identical role. PAR2 inhibitor blocked these processes. The effectiveness of rabeprazole was outperformed by the addition of a PAR2 inhibitor. CONCLUSION: Trypsin in reflux can cause GERD by activating the PAR2 and NLRP3 inflammasome pathway, which impairs the esophageal mucosal barrier. Our research will aid in the identification of potential targets for the treatment of GERD.

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L-theanine attenuates porcine intestinal tight junction damage induced by LPS via p38 MAPK/NLRP3 signaling in IPEC-J2 cells

Cited by 9 publications

References 27 publications

Ziziphus jujuba Miller Ethanol Extract Restores Disrupted Intestinal Barrier Function via Tight Junction Recovery and Reduces Inflammation

Ziziphus jujuba Miller Ethanol Extract Restores Disrupted Intestinal Barrier Function via Tight Junction Recovery and Reduces Inflammation

Galangin Prevents Against Ethanol-Induced Intestinal Barrier Dysfunction and NLRP3 Inflammasome Activation via NF-κB/MAPK Signaling Pathways in Mice and Caco-2 Cells

Trypsin activates PAR2 inhibits the expression of tight junction protein through activation of NLRP3 inflammasome pathway in gastroesophageal reflux disease

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