Effects of Qing Hua Chang Yin on lipopolysaccharide‑induced intestinal epithelial tight junction injury in Caco‑2 cells

Fang, Wenyi; Zhao, Peilin; Shen, Aling; Liu, Liya; Chen, Hongwei; Chen, Youqin; Peng, Jun; Sferra, Thomas J.; Sankararaman, Senthilkumar; Luo, Yunfeng; Ke, Xiao

doi:10.3892/mmr.2021.11844

Cited by 13 publications

(13 citation statements)

References 33 publications

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“…To corroborate the results obtained from in vivo assays, we established an in vitro model by stimulating Caco‐2 cells using LPS, a commonly used cell model in the studies of IBDs 45–47 . The cells challenged with LPS exhibited decreased proliferation, enhanced apoptosis, elevated expression of pro‐inflammatory cytokines, and increased oxidative stress, suggesting the successful establishment of the cell model.…”

Section: Discussionmentioning

confidence: 74%

“…To corroborate the results obtained from in vivo assays, we established an in vitro model by stimulating Caco-2 cells using LPS, a commonly used cell model in the studies of IBDs. [45][46][47] The cells challenged with LPS exhibited decreased proliferation, enhanced apoptosis, elevated expression of pro-inflammatory cytokines, and increased oxidative stress, suggesting the successful establishment of the cell model. After treating with daphnetin, the stimulated inflammation and oxidative stress in LPS-challenged cells were substantially suppressed, further supporting the results from in vivo experiments.…”

Section: Discussionmentioning

confidence: 99%

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Daphnetin attenuates intestinal inflammation, oxidative stress, and apoptosis in ulcerative colitis via inhibiting REG3A‐dependent JAK2/STAT3 signaling pathway

Liu

2023

Environmental Toxicology

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Daphnetin is a natural coumarin compound with anti‐inflammatory, anti‐oxidant, and anti‐apoptotic effects, which has been previously demonstrated to ameliorate DSS‐induced ulcerative colitis (UC). However, the molecular mechanism involved in the daphnetin‐mediated pathological process of UC remains unclarified. The current study used DSS‐induced mice and LPS‐challenged Caco‐2 cells as UC models. Bodyweight, disease activity index (DAI) score, and colon length were used to evaluate the severity of colitis. The histological changes in colon tissues were observed using H&E and PAS staining. Protein levels were detected by western blot. The malondialdehyde (MDA) and superoxide dismutase (SOD) activities were used to assess oxidative stress. Inflammatory responses were evaluated by detecting the levels of inflammatory cytokines (IFN‐r, IL‐1β, IL‐6, and TNF‐α) using flow cytometry. CCK‐8 and TUNEL assay were employed to determine cell growth and cell death, respectively. The results showed that daphnetin could ameliorate the severity of colitis and attenuate the damage to intestinal structure in DSS‐induced mice. Compared with the DSS group, the expression of ZO‐1, occludin, and anti‐apoptotic protein (BCL‐2) was increased while the level of pro‐apoptotic proteins (Bax and cleaved caspase 3) was decreased in DSS + daphnetin group. The activity of MDA and SOD, as well as the levels of inflammatory cytokines were substantially suppressed by daphnetin. In consistency, in vitro assays indicated that daphnetin protected Caco‐2 cells from LPS‐stimulated viability impairment, apoptosis, oxidative stress, and inflammation. Furthermore, daphnetin suppressed the activity of JAK2/STAT signaling in LPS‐induced Caco‐2 cells in a REG3A‐dependent manner. REG3A overexpression abated the ameliorative effects of daphnetin while JAK2/STAT signaling inhibition functioned synergically with daphnetin in LPS‐stimulated Caco‐2 cells. Collectively, this study deepened the understanding of the therapeutic effects of daphnetin on UC and uncovered for the first time that daphnetin functioned through REG3A‐activated JAK2/STAT3 signaling in UC, which may provide novel insights for the treatment of UC.

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Section: Discussionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 99%

Daphnetin attenuates intestinal inflammation, oxidative stress, and apoptosis in ulcerative colitis via inhibiting REG3A‐dependent JAK2/STAT3 signaling pathway

Liu

2023

Environmental Toxicology

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“…The cells were then treated with culture medium (1 mL/well) for 24 h. Subsequently, cells in every group were either stimulated with 1 µg/mL of LPS from Escherichia coli , serotype 055:B5 (Sigma Chemical Company, Saint Louis, MO, USA) for 30 min (western blotting assay) or 24 h (cell viability assay, cytokine measurement in the cell supernatant, glutathione peroxidase activity, and intracellular reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio. The chosen dose of LPS was based on a study [ 21 ] that demonstrated that 1 μg/mL of LPS induces the production of IL-8 from Caco-2 cells, and this dose does not affect Caco-2 cell viability [ 22 ].…”

Section: Methodsmentioning

confidence: 99%

Effects of Branched-Chain Amino Acids on the Inflammatory Response Induced by LPS in Caco-2 Cells

Garcia,

Makiyama,

Sampaio

et al. 2024

Metabolites

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Branched-chain amino acids (BCAA) are essential for maintaining intestinal mucosal integrity. However, only a few studies have explored the role of BCAA in the modulation of intestinal inflammation. In this study, we investigated in vitro effects of BCAA on the inflammatory response induced by lipopolysaccharide (LPS) (1 µg/mL) in Caco-2 cells. Caco-2 cells were assigned to six groups: control without BCAA (CTL0), normal BCAA (CTL; 0.8 mM leucine, 0.8 mM isoleucine, and 0.8 mM valine); leucine (LEU; 2 mM leucine), isoleucine (ISO; 2 mM isoleucine), valine (VAL; 2 mM valine), and high BCAA (LIV; 2 mM leucine, 2 mM isoleucine, and 2 mM valine). BCAA was added to the culture medium 24 h before LPS stimulation. Our results indicated that BCAA supplementation did not impair cell viability. The amino acids leucine and isoleucine attenuated the synthesis of IL-8 and JNK and NF-kB phosphorylation induced by LPS. Furthermore, neither BCAA supplementation nor LPS treatment modulated the activity of glutathione peroxidase or the intracellular reduced glutathione/oxidized glutathione ratio. Therefore, leucine and isoleucine exert anti-inflammatory effects in Caco-2 cells exposed to LPS by modulating JNK and NF-kB phosphorylation and IL-8 production. Further in vivo studies are required to validate these findings and gather valuable information for potential therapeutic or dietary interventions.

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“…In dextran sulfate sodium (DSS)-induced UC mice, the QingBai decoction, Huang-Lian-Jie-Du Decoction, and Huangqin Decoction increased the expression of ZO-1 and Occludin in colonic mucosal [ 13 – 15 ]. Fang investigated the effect of Qing Hua Chang Yin on the loss of intestinal epithelial barrier integrity induced by lipopolysaccharide (LPS) in vitro using a Caco-2 cell model and found that Qing Hua Chang Yin could upregulate the mRNA and protein expression levels of Claudin-1 [ 16 ]. In addition, Sijunzi Decoction can also upregulate the level of Claudin-2 in the colon tissue of rats induced by a 2,4,6-trinitrobenzene sulfonic acid (TNBS) in vivo as an intestinal barrier protector [ 17 ].…”

Section: Intestinal Mucosal Barriermentioning

confidence: 99%

Inflammatory bowel disease: an overview of Chinese herbal medicine formula-based treatment

Yuan

Wang

et al. 2022

Chin Med

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Inflammatory bowel disease (IBD) is a chronic recurrent inflammatory disease of the intestine, including Crohn’s disease (CD) and ulcerative colitis (UC), whose etiology and pathogenesis have not been fully understood. Due to its prolonged course and chronic recurrence, IBD imposes a heavy economic burden and psychological stress on patients. Traditional Chinese Herbal Medicine has unique advantages in IBD treatment because of its symptomatic treatment. However, the advantages of the Chinese Herbal Medicine Formula (CHMF) have rarely been discussed. In recent years, many scholars have conducted fundamental studies on CHMF to delay IBD from different perspectives and found that CHMF may help maintain intestinal integrity, reduce inflammation, and decrease oxidative stress, thus playing a positive role in the treatment of IBD. Therefore, this review focuses on the mechanisms associated with CHMF in IBD treatment. CHMF has apparent advantages. In addition to the exact composition and controlled quality of modern drugs, it also has multi-component and multi-target synergistic effects. CHMF has good prospects in the treatment of IBD, but its multi-agent composition and wide range of targets exacerbate the difficulty of studying its treatment of IBD. Future research on CHMF-related mechanisms is needed to achieve better efficacy.

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Effects of Qing Hua Chang Yin on lipopolysaccharide‑induced intestinal epithelial tight junction injury in Caco‑2 cells

Cited by 13 publications

References 33 publications

Daphnetin attenuates intestinal inflammation, oxidative stress, and apoptosis in ulcerative colitis via inhibiting REG3A‐dependent JAK2/STAT3 signaling pathway

Daphnetin attenuates intestinal inflammation, oxidative stress, and apoptosis in ulcerative colitis via inhibiting REG3A‐dependent JAK2/STAT3 signaling pathway

Effects of Branched-Chain Amino Acids on the Inflammatory Response Induced by LPS in Caco-2 Cells

Inflammatory bowel disease: an overview of Chinese herbal medicine formula-based treatment

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