α-Chaconine Affects the Apoptosis, Mechanical Barrier Function, and Antioxidant Ability of Mouse Small Intestinal Epithelial Cells

He, Yi; Chen, Jiaqi; Zhang, Qiyue; Zhang, Jialong; Wang, Lulai; Chen, Xiaoxia; Molenaar, Adrian; Sun, Xuezhao

doi:10.3389/fpls.2021.673774

Cited by 10 publications

(11 citation statements)

References 59 publications

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“…During the differentiation process of Caco-2 cells, the cells continuously secrete the marker enzyme-IAP to the AP side. When the ratio of IAP activity in the AP side and BP side is over 3, indicating that the monolayer barrier is relatively complete ( He et al, 2021 ). TEER is one of the best methods for assessing tight junction integrity in the Caco-2 cell monolayers model.…”

Section: Resultsmentioning

confidence: 99%

“…Intestinal alkaline phosphatase (IAP) is a marker enzyme of the brush edge of small intestinal epithelia, which can be used to evaluate the differentiation state of cell ( He et al, 2021 ). At 7, 14, and 21 days after inoculation, the culture medium of AP and BP side was taken, and the IAP activity was measured according to the instructions in the kit (Nanjing jiancheng bioengineering institute, Jiangsu, China).…”

Section: Methodsmentioning

confidence: 99%

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Relief Effects of Icariin on Inflammation-Induced Decrease of Tight Junctions in Intestinal Epithelial Cells

Liu²,

Pongkorpsakol³

et al. 2022

Front. Pharmacol.

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Inflammatory cytokines including TNF-α and IL-1β impair intestinal barrier function in aging by disrupting intestinal tight junction integrity. Icariin (ICA) has a variety of pharmacological effects. Indeed, ICA produces anti-inflammatory, anti-oxidative stress, and inhibitory effects on microRNA (miRNA) expression. This study was to explore whether ICA could alleviate inflammation-associated intestinal barrier function impairment in aging and its underlying mechanism. Of particular interest, network pharmacology prediction indicated the potential therapeutic impacts of ICA for the treatment of colitis. Then, rats were used to study whether ICA has a protective effect on the reduction of tight junctions caused by inflammatory cytokines. Next, Caco-2 cell monolayers were used to explore the mechanism by which ICA alleviates the down-regulation of tight junctions. Network pharmacology prediction revealed that ICA alleviated colitis via suppressing oxidative stress. After ICA intervention, expressions of inflammatory cytokines were reduced, but tight junctions, antioxidant enzymes in aging rats were up-regulated. ICA reversed the TNF-α-induced decrease in abundance of Occludin protein in Caco-2 cell monolayers. Meanwhile, ICA alleviated the increase in permeability and expression of miR-122a. However, the protective effect of ICA was markedly attenuated after transfection with miR-122a mimics. In conclusion, ICA reduced the expressions of Occludin, Claudin1, and Claudin5 in colon, which were related to the reduction of TNF-α and IL-1β and alleviation of colonic in vivore. And ICA attenuated TNF-α-induced Occludin disruption and epithelial barrier impairment by decreasing miR-122a expression in Caco-2 cell monolayers.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Relief Effects of Icariin on Inflammation-Induced Decrease of Tight Junctions in Intestinal Epithelial Cells

Liu²,

Pongkorpsakol³

et al. 2022

Front. Pharmacol.

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“…Intestinal epithelial cells have barrier functions such as tight junctions, preventing the invasion of certain toxins from penetrating the intestine [ 26 ]. Next, we further investigated the protective potential of acidifiers on the barrier function of small intestinal epithelial cells after oxidative stress induced by DQ.…”

Section: Resultsmentioning

confidence: 99%

Acidifiers Attenuate Diquat-Induced Oxidative Stress and Inflammatory Responses by Regulating NF-κB/MAPK/COX-2 Pathways in IPEC-J2 Cells

Liu

Chao

et al. 2022

Antioxidants

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In this study, we evaluated the protective effects and potential mechanisms of acidifiers on intestinal epithelial cells exposure to oxidative stress (OS). IPEC-J2 cells were first pretreated with 5 × 10−5 acidifiers for 4 h before being exposed to the optimal dose of diquat to induce oxidative stress. The results showed that acidifiers attenuated diquat-induced oxidative stress, which manifests as the improvement of antioxidant capacity and the reduction in reactive oxygen species (ROS) accumulation. The acidifier treatment decreased cell permeability and enhanced intestinal epithelial barrier function through enhancing the expression of claudin-1 and occludin in diquat-induced cells. Moreover, acidifier treatment attenuated diquat-induced inflammatory responses, which was confirmed by the decreased secretion and gene expression of pro-inflammatory (TNF-α, IL-8) and upregulated anti-inflammatory factors (IL-10). In addition, acidifiers significantly reduced the diquat-induced gene and protein expression levels of COX-2, NF-κB, I-κB-β, ERK1/2, and JNK2, while they increased I-κB-α expression in IPEC-J2 cells. Furthermore, we discovered that acidifiers promoted epithelial cell proliferation (increased expression of PCNA and CCND1) and inhibited apoptosis (decreased expression of BAX, increased expression of BCL-2). Taken together, these results suggest that acidifiers are potent antioxidants that attenuate diquat-induced inflammation, apoptosis, and maintain cellular barrier integrity by regulating the NF-κB/MAPK/COX-2 signaling pathways.

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“…There were a large number of TUNEL + cells in the crypts and villi in WAI group compared to the CON group, and EGCG+WAI group significantly decreased the apoptosis levels in the small intestine (Figure 3f). Alkaline phosphatase (ALP) is an endogenous enzyme and plays an important role in maintaining the integrity of intestinal epithelial cells (He et al, 2021; Sheng et al, 2021). At 3.5 days after WAI, ALP was lost from the jejunal (Figure 3g), the permeability of epithelial cells increased, causing increasingly expression of inflammatory factors (Figure 3h-j) (Lallès, 2019).…”

Section: Resultsmentioning

confidence: 99%

The radio-protective effects of (-)- Epigallocatechin-3-gallate (EGCG): regulating macrophage function in radiation-induced intestinal injury

Tang

et al. 2022

Preprint

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Accidental and medical radiation exposure may cause radiation-induced intestinal injury (RIII), a catastrophic disease requiring efficient therapies. (-)-Epigallocatechin-3-gallate (EGCG), a major constituent of green tea, has been shown to have potent biological activity as well as strong anti-inflammation effects. Here, we demonstrate that EGCG treatment not only protects mice against total body irradiation (TBI)-induced toxicity and weight loss but also alleviates whole abdominal irradiation (WAI)- induced intestinal injury. EGCG promotes proliferation and survival of intestinal stem cells, inhibits radiation-induced apoptosis and inflammation. At the same time, EGCG preserves the composition of the gut microbiota in WAI mice. In vitro, we demonstrate that EGCG regulates the release of radiation-induced inflammatory factors by inhibiting inflammatory pathways such as toll-like receptor signaling pathway in peritoneal macrophages. Mechanistically, the radioprotective effect of EGCG was likely attributable to its preservation on macrophages and the colonized gut microbiota composition, thus relieving the intestinal inflammation. EGCG provides a novel strategy to mitigate RIII and improve the prognosis of patients after radiotherapy.

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α-Chaconine Affects the Apoptosis, Mechanical Barrier Function, and Antioxidant Ability of Mouse Small Intestinal Epithelial Cells

Cited by 10 publications

References 59 publications

Relief Effects of Icariin on Inflammation-Induced Decrease of Tight Junctions in Intestinal Epithelial Cells

Relief Effects of Icariin on Inflammation-Induced Decrease of Tight Junctions in Intestinal Epithelial Cells

Acidifiers Attenuate Diquat-Induced Oxidative Stress and Inflammatory Responses by Regulating NF-κB/MAPK/COX-2 Pathways in IPEC-J2 Cells

The radio-protective effects of (-)- Epigallocatechin-3-gallate (EGCG): regulating macrophage function in radiation-induced intestinal injury

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