Benzo[a]pyrene induces epithelial tight junction disruption and apoptosis via inhibiting the initiation of autophagy in intestinal porcine epithelial cells

Li, Jun; Bai, Jun; Si, Xuemeng; Hai, Jian; Wu, Zhenlong

doi:10.1016/j.cbi.2023.110386

Cited by 10 publications

(5 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The intestinal barrier is the first defense wall to resist bacterial infection, enhancing the function of intestinal barrier becomes the therapeutic strategy for preventing intestinal diseases (Wu et al, 2019). The abundance of TJ protein is an important indicator for evaluating intestinal function (Li et al, 2023). Previous study has demonstrated that treatment with LPS decreased the mRNA levels and protein expression in IPEC‐J2 cells (He et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Tert‐butylhydroquinone attenuates LPS‐induced pyroptosis of IPEC‐J2 cells via downregulating HMGB1/TLR4/NF‐κB axis

Qiu,

Zhang,

Pang

et al. 2023

Animal Physiology Nutrition

View full text Add to dashboard Cite

Inflammatory response induced by biological stress usually occurs in weaning piglets, it reduces the production performance of piglets and even causes death. Tert‐butylhydroquinone (TBHQ) is a food additive that has the effect of anti‐inflammation and anti‐oxidation. However, there are few reports related to the protective mechanisms of TBHQ on lipopolysaccharide (LPS) induced injury in intestinal porcine epithelial (IPEC‐J2) cells. Quantitative real‐time polymerase chain reaction and western blot analysis, respectively, detected the mRNA levels and protein expressions related to pyroptosis, tight junction (TJ) protein and high‐mobility group box 1/toll‐like receptor 4/nuclear factor kappa‐B (HMGB1/TLR4/NF‐κB) axis. Localisation and expression of NOD‐like receptor pyrin domain containing 3 (NLRP3), HMGB1 and P‐NF‐κB proteins detected by immunofluorescence. The results showed that TBHQ (12.5 and 25 μM) can increase cell activity and reduce intracellular lactate dehydrogenase (LDH) levels in a dose‐dependent manner. LPS significantly decreases cell viability and increases the LDH level. However, pretreatment with TBHQ evidently increases cell viability and decreases the LDH level of IPEC‐J2 cells. In addition, treatment with LPS decreased the mRNA level and protein expression of zonula occludens‐1, occludin and claudin‐1, and increased the mRNA level and protein expression of pyroptosis and HMGB1/TLR4/NF‐κB axis. Interestingly, pretreatment with TBHQ increased the TJ protein expressions as well as decreased the mRNA level and protein expressions of pyroptosis and HMGB1/TLR4/NF‐κB axis. Moreover, the results of immunofluorescence showed that TBHQ significantly reduced the expression of NLRP3, HMGB1 and P‐NF‐κB in LPS‐induced injury of IPEC‐J2 cells. Therefore, we come to the conclusion that TBHQ attenuates LPS‐induced pyroptosis in IPEC‐J2 cells through downregulation of the HMGB1/TLR4/NF‐κB axis, TBHQ may become a potential feed additive for preventing inflammatory diarrhoea in piglets.

show abstract

Section: Discussionmentioning

confidence: 99%

Tert‐butylhydroquinone attenuates LPS‐induced pyroptosis of IPEC‐J2 cells via downregulating HMGB1/TLR4/NF‐κB axis

Qiu,

Zhang,

Pang

et al. 2023

Animal Physiology Nutrition

View full text Add to dashboard Cite

show abstract

“…The colon tissue was homogenized in liquid nitrogen and lysed in a RIPA buffer for protein extraction. Protein abundance was assayed using western blotting as previously described . The supernatant was harvested after centrifuging at 12,000 g for 15 min, and protein abundance was assayed using the bicinchoninic acid (BCA) method.…”

Section: Methodsmentioning

confidence: 99%

“…Protein abundance was assayed using western blotting as previously described. 33 The supernatant was harvested after centrifuging at 12,000g for 15 min, and protein abundance was assayed using the bicinchoninic acid (BCA) method. Denatured proteins were separated using SDS-PAGE, transferred onto a PVDF membrane (Millipore, Billerica, MA, USA), and probed with the appropriate antibodies.…”

Section: Evaluation Of Serum Oxidative Stressmentioning

confidence: 99%

An Isofibrous Diet with Fiber Konjac Glucomannan Ameliorates Salmonella typhimurium-Induced Colonic Injury by Regulating TLR2-NF-κB Signaling and Intestinal Microbiota in Mice

Li,

Liu,

et al. 2024

J. Agric. Food Chem.

Self Cite

View full text Add to dashboard Cite

This study aimed to investigate the hypothesis that dietary konjac glucomannan (KGM) could alleviate Salmonella typhimurium-induced colitis by modulating intestinal microbiota. Mice were fed an isocaloric and isofibrous diet supplemented with either 7% KGM or cellulose and were treated with 5 × 108 CFU of S. typhimurium. The results showed that KGM had an average molecular weight of 936 kDa and predominantly consisted of mannose and glucose at a molar ratio of 1:1.22. In vivo studies demonstrated that dietary KGM effectively mitigated colonic lesions, oxidative stress, disruption of tight junction protein 2 and occludin, and the inflammatory response induced by S. typhimurium. Moreover, KGM administration alleviated the dramatic upregulation of toll-like receptor 2 (TLR2) and phosphonuclear factor κB (NF-κB) protein abundance, induced by Salmonella treatment. Notably, dietary KGM restored the reduced Muribaculaceae and Lactobacillus abundance and increased the abundance of Blautia and Salmonella in S. typhimurium-infected mice. Spearman correlation analysis revealed that the gut microbiota improved by KGM contribute to inhibit inflammation and oxidative stress. These results demonstrated the protective effects of dietary KGM against colitis by modulating the gut microbiota and the TLR2-NF-κB signaling pathway in response to Salmonella infection.

show abstract

“…Furthermore, Kim et al [ 13 ] discovered that protease-activated receptor 2 regulates autophagy and intestinal epithelial TJs, thus reducing intestinal epithelial permeability. Additionally, another study discovered that rapamycin (autophagy inducer) dramatically improved intestinal damage in benzo[a]pyrene induced intestinal epithelial TJ disruption[ 14 ]. In conclusion, the activation of autophagy plays an important role in maintaining intestinal barrier function against toxic chemicals, intestinal inflammation, and intestinal permeability.…”

Section: Autophagy and Gi Physical Barrier Functionmentioning

confidence: 99%

Morphological and biochemical characteristics associated with autophagy in gastrointestinal diseases

Chang,

Li,

Liu

et al. 2024

World J Gastroenterol

View full text Add to dashboard Cite

Autophagy is a cellular catabolic process characterized by the formation of double-membrane autophagosomes. Transmission electron microscopy is the most rigorous method to clearly visualize autophagic engulfment and degradation. A large number of studies have shown that autophagy is closely related to the digestion, secretion, and regeneration of gastrointestinal (GI) cells. However, the role of autophagy in GI diseases remains controversial. This article focuses on the morphological and biochemical characteristics of autophagy in GI diseases, in order to provide new ideas for their diagnosis and treatment.

show abstract

Benzo[a]pyrene induces epithelial tight junction disruption and apoptosis via inhibiting the initiation of autophagy in intestinal porcine epithelial cells

Cited by 10 publications

References 44 publications

Tert‐butylhydroquinone attenuates LPS‐induced pyroptosis of IPEC‐J2 cells via downregulating HMGB1/TLR4/NF‐κB axis

Tert‐butylhydroquinone attenuates LPS‐induced pyroptosis of IPEC‐J2 cells via downregulating HMGB1/TLR4/NF‐κB axis

An Isofibrous Diet with Fiber Konjac Glucomannan Ameliorates Salmonella typhimurium-Induced Colonic Injury by Regulating TLR2-NF-κB Signaling and Intestinal Microbiota in Mice

Morphological and biochemical characteristics associated with autophagy in gastrointestinal diseases

Contact Info

Product

Resources

About