1,25-Dihydroxyvitamin D3 preserves intestinal epithelial barrier function from TNF-α induced injury via suppression of NF-kB p65 mediated MLCK-P-MLC signaling pathway

Chen, Shanwen; Zhu, Jing; Chen, Guowei; Zuo, Shuai; Zhang, Junling; Chen, Ziyi; Wang, Xin; Li, Junxia; Liu, Yucun; Wang, Pengyuan

doi:10.1016/j.bbrc.2015.03.125

Cited by 65 publications

(45 citation statements)

References 33 publications

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“…The results demonstrated that EEDAR-H reduced the phosphorylation of p38 by inhibiting the expression of PAR-2. MLCK can promote the phosphorylation of MLC, induce contraction of actin and myosin, promote the endocytosis of Occludin and other proteins, and then cause the translocation and reduction of tight junction proteins [44][45][46]. The results of the present study demonstrated that EEDAR inhibited both P-MLC and MLCK.…”

Section: Discussionsupporting

confidence: 56%

Deep-Fried Atractylodis Rhizoma Protects against Spleen Deficiency-Induced Diarrhea through Regulating Intestinal Inflammatory Response and Gut Microbiota

Shi

Xiong

et al. 2019

IJMS

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According to the theories of traditional Chinese medicine, spleen deficiency often leads to diarrhea, and deep-fried Atractylodis Rhizoma (DAR) is commonly used for the treatment. However, the association between spleen deficiency and diarrhea remains unclear. The present study aimed to investigate the therapeutic effect of DAR for the treatment of diarrhea caused by spleen deficiency and analyze the related mechanisms. It was found that a high dose group of an ethanolic extract of deep-fried Atractylodis Rhizoma (EEDAR-H) significantly inhibited weight loss, diarrhea, and pathological changes in colon tissue induced by rhubarb. EEDAR-H was found to significantly reduce the level of intestinal inflammatory cytokines and increase the expression of gastrointestinal motility hormones. In addition, EEDAR-H significantly increased the expression of aquaporin 3 (AQP3) and aquaporin 8 (AQP8) and restored abnormal water metabolism; Shen-Ling-Bai-Zhu-San (SLBZS) induced the same effect as EEDAR-H. Additional tests on the mechanism found that EEDAR-H and SLBZS promoted the integrity of the intestinal barrier. Both significantly increased the expression of the tight junction protein ZO-1 and Occludin, inhibited the phosphorylation of p38MAPK and MLC, and significantly reduced the expression levels of PAR-2. Analysis of the gut microbiota indicated that overall changes in its structure were reversed after treatment with EEDAR-H or SLBZS, in addition to significant modulation of the abundance of different phyla. At the genus level, EEDAR-H or SLBZS significantly reduced the levels of potential pathogens and increased those of beneficial bacteria.

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Section: Discussionsupporting

confidence: 56%

Deep-Fried Atractylodis Rhizoma Protects against Spleen Deficiency-Induced Diarrhea through Regulating Intestinal Inflammatory Response and Gut Microbiota

Shi

Xiong

et al. 2019

IJMS

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“…Vitamin D could restore intestinal barrier injury induced by ethanol through the redistribution of TJ proteins, lowering the phosphorylation level of myosin light chain, and decreasing the generation of ROS (24). Suppression of the nuclear factor-κB pathway also contributed to the protective effect of vitamin D (25). There might be other mechanisms of the intestinal-protective effect of vitamin D in NEC.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D ameliorates neonatal necrotizing enterocolitis via suppressing TLR4 in a murine model

et al. 2018

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BACKGROUND: The toll-like receptor 4 (TLR4) has been reported to play an important role in necrotizing enterocolitis (NEC). As an established regulator of TLR4, vitamin D has been demonstrated to be intestinal-protective. This study aims at finding out whether the vitamin D/vitamin D receptor (VDR) pathway ameliorates NEC by regulating TLR4. METHODS: Serum 25-hydrovitamin D (25(OH)D) was tested and compared in 15 preterm infants with NEC, 12 preterm infants without known complications and 20 healthy term infants. Neonatal Wistar rats were grouped and NEC was induced through formula feeding and cold/asphyxia stress. Vitamin D and the vehicle were administered to compare the microscopic structure, apoptotic protein expression, intestinal barrier function, inflammatory response, and TLR4 expression. RESULTS: Preterm infants with NEC had significantly lower 25 (OH)D levels than those without NEC and healthy subjects. VDR expression was suppressed, whereas TLR4 expression was elevated in the NEC intestine. Vitamin D may increase the survival rate, alleviate structure damage, and preserve intestinal barrier function. These were achieved partly through restoration of VDR and suppression of TLR4. CONCLUSION: NEC infants have lower levels of vitamin D. The vitamin D/VDR pathway protects against intestinal injury of NEC partly through suppressing the expression of TLR4.

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“…The closer the P-value is to zero, the greater the Rich factor is. The greater the Gene Number is, the more the enrichment is significant be activated by TGEV infection [21][22][23][24][25][26][27]. RIG-I is a dsRNA helicase enzyme encoded by the DDX58 gene and recognizes viral double-stranded (ds) RNA to interfere with viral infection [28,29].…”

Section: Discussionmentioning

confidence: 99%

Differentially expressed non-coding RNAs induced by transmissible gastroenteritis virus potentially regulate inflammation and NF-κB pathway in porcine intestinal epithelial cell line

Zhao

Zhang

et al. 2018

BMC Genomics

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BackgroundTransmissible gastroenteritis virus (TGEV) infection can activate NF-κB pathway in porcine intestinal epithelial cells and result in severe inflammation. Non-coding RNAs (ncRNAs) are not translated into proteins and play an important role in many biological and pathological processes such as inflammation, viral infection, and mitochondrial damage. However, whether ncRNAs participate in TGEV-induced inflammation in porcine intestinal epithelial cells is largely unknown.ResultsIn this study, the next-generation sequencing (NGS) technology was used to analyze the profiles of mRNAs, miRNAs, and circRNAs in Mock- and TGEV-infected intestinal porcine epithelial cell-jejunum 2 (IPEC-J2) cell line. A total of 523 mRNAs, 65 microRNAs (miRNAs), and 123 circular RNAs (circRNAs) were differentially expressed. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed differentially expressed mRNAs were linked to inflammation-related pathways, including NF-κB, Toll-like receptor, NOD-like receptor, Jak-STAT, TNF, and RIG-I-like receptor pathways. The interactions among mRNA, miRNA, and circRNA were analyzed. The data showed that ssc_circ_009380 and miR-22 might have interaction relationship. Dual-luciferase reporter assay confirmed that miR-22 directly bound to ssc_circ_009380. We also observed that overexpression of miR-22 led to a reduction of p-IκB-α and accumulation of p65 in nucleus in TGEV-infected IPEC-J2 cells. In contrast, inhibition of miR-22 had the opposite effects. Moreover, silencing of ssc_circ_009380 inhibited accumulation of p65 in nucleus and phosphorylation of IκB-α.ConclusionsThe data revealed that differentially expressed mRNAs and ncRNAs were primarily enriched in inflammation-related pathways and ssc_circ_009380 promoted activation of NF-κB pathway by binding miR-22 during TGEV-induced inflammation.Electronic supplementary materialThe online version of this article (10.1186/s12864-018-5128-5) contains supplementary material, which is available to authorized users.

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1,25-Dihydroxyvitamin D3 preserves intestinal epithelial barrier function from TNF-α induced injury via suppression of NF-kB p65 mediated MLCK-P-MLC signaling pathway

Cited by 65 publications

References 33 publications

Deep-Fried Atractylodis Rhizoma Protects against Spleen Deficiency-Induced Diarrhea through Regulating Intestinal Inflammatory Response and Gut Microbiota

Deep-Fried Atractylodis Rhizoma Protects against Spleen Deficiency-Induced Diarrhea through Regulating Intestinal Inflammatory Response and Gut Microbiota

Vitamin D ameliorates neonatal necrotizing enterocolitis via suppressing TLR4 in a murine model

Differentially expressed non-coding RNAs induced by transmissible gastroenteritis virus potentially regulate inflammation and NF-κB pathway in porcine intestinal epithelial cell line

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