The Effects of Lauric Acid on IPEC-J2 Cell Differentiation, Proliferation, and Death

2020 ◽  
Vol 20 (7) ◽  
pp. 572-581
Author(s):  
Yuan Yang ◽  
Jin Huang ◽  
Jianzhong Li ◽  
Huansheng Yang ◽  
Yulong Yin
Keyword(s):  
Cell Death ◽  
Cell Differentiation ◽  
Cell Viability ◽  
P38 Mapk ◽  
Lauric Acid ◽  
Cell Apoptosis ◽  
Epithelial Cell Line ◽  
Intestinal Epithelial ◽  
Metabolism Regulation ◽  
Cell Proliferation Inhibition

Background: Lauric acid (LA) has antimicrobial effects and the potential to replace antibiotics in feeds to prevent postweaning diarrhea and increase overall swine productivity. The effects of lauric acid on the intestinal epithelial cells remain unclear. Materials and Methods: This study investigates the effects of LA on pig intestinal epithelial cell line (IPEC-J2) differentiation, proliferation, and death and explores its underlying mechanisms. It was found that 0.25-0.1 mM LA promoted IPEC-J2 cell differentiation. At 1 mM or higher concentrations, it induced IPEC-J2 cell viability decreases, lipid accumulation, cell proliferation inhibition, and cell apoptosis. The cell death induced did not depend on caspase pathways. : The data demonstrated that LA induced the IPEC-J2 cell autophagy and impaired autophagy flux and autophagy plays a role in protecting against LA induced-cell death. p38 MAPK inhibitor SB202190 attenuated LA-reduced IPEC-J2 cell viability. This associated with an increase in autophagy level and a decrease in lipid accumulations and FABPI levels. Conclusion: Conclusion: In summary, LA promoted the IPEC-J2 cell apoptosis depends on the p38 MAPK pathways and may involve autophagy and TG metabolism regulation.

The Effects of Butyric Acid on the Differentiation, Proliferation, Apoptosis, and Autophagy of IPEC-J2 Cells

2020 ◽  
Vol 20 (4) ◽  
pp. 307-317
Author(s):  
Yuan Yang ◽  
Jin Huang ◽  
Jianzhong Li ◽  
Huansheng Yang ◽  
Yulong Yin
Keyword(s):  
Cell Viability ◽  
P38 Mapk ◽  
Butyric Acid ◽  
Cell Apoptosis ◽  
Mapk Pathway ◽  
Mrna Level ◽  
Dependent Manner ◽  
M Phase ◽  
High Concentrations ◽  
Underlying Mechanisms

Background: Butyric acid (BT), a short-chain fatty acid, is the preferred colonocyte energy source. The effects of BT on the differentiation, proliferation, and apoptosis of small intestinal epithelial cells of piglets and its underlying mechanisms have not been fully elucidated. Methods: In this study, it was found that 0.2-0.4 mM BT promoted the differentiation of procine jejunal epithelial (IPEC-J2) cells. BT at 0.5 mM or higher concentrations significantly impaired cell viability in a dose- and time-dependent manner. In addition, BT at high concentrations inhibited the IPEC-J2 cell proliferation and induced cell cycle arrest in the G2/M phase. Results: Our results demonstrated that BT triggered IPEC-J2 cell apoptosis via the caspase8-caspase3 pathway accompanied by excess reactive oxygen species (ROS) and TNF-α production. BT at high concentrations inhibited cell autophagy associated with increased lysosome formation. It was found that BT-reduced IPEC-J2 cell viability could be attenuated by p38 MAPK inhibitor SB202190. Moreover, SB202190 attenuated BT-increased p38 MAPK target DDIT3 mRNA level and V-ATPase mRNA level that were responsible for normal acidic lysosomes. Conclusion: In conclusion, 1) at 0.2-0.4 mM, BT promotes the differentiation of IPEC-J2 cells; 2) BT at 0.5 mM or higher concentrations induces cell apoptosis via the p38 MAPK pathway; 3) BT inhibits cells autophagy and promotes lysosome formation at high concentrations.

scholarly journals Methyl jasmonate reduces the inflammation and apoptosis of HK-2 cells induced by LPS by regulating the NF-κB pathway

2021 ◽  
Keyword(s):  
Cell Viability ◽  
Methyl Jasmonate ◽  
Cell Apoptosis ◽  
Cell Model ◽  
Tubular Epithelial Cell ◽  
Cell Protein ◽  
Epithelial Cell Line ◽  
Tnf Α ◽  
Iκbα Phosphorylation ◽  
Anti Inflammatory

Background: Methyl jasmonate is a bioactive oxylipid that participates in the defense-related mechanisms of plants. The anti-inflammatory and anti-oxidative capacities of methyl jasmonate against lipopolysaccharide (LPS) induced arthritis have been widely investigated. However, the role of methyl jasmonate in LPS-induced cell model of tubular-interstitial nephritis (TIN) has not been reported. Methods: LPS (5 µg/mL) was applied to treat human renal tubular epithelial cell line (HK-2) for the establishment of TIN cell model. LPS-induced HK-2 was incubated with 10 or 20 µM methyl jasmonate, cell viability and apoptosis were assessed by MTT and flow cytometry. ELISA and qRT-PCR were performed to determine the levels of interleukin (IL)-1 beta (IL-1β), IL-6, IL-8 and tumor necrosis factor-α (TNF-α). The downstream pathway was investigated by western blot. Results: LPS induced cytotoxicity in HK-2 cell accompanied by decrease of cell viability and increase of cell apoptosis. Methyl jasmonate dosage dependently enhanced the cell viability and reduced cell apoptosis to ameliorate the cytotoxicity. LPS also induced inflammatory response in HK-2 cell with increased IL-1β, IL-6, IL-8 and TNF-α. Methyl jasmonate attenuated LPS-induced inflammation in HK-2 cell. Protein expression of IκBα was down-regulated, p65 and IκBα phosphorylation were up-regulated in LPS-induced HK-2. Methyl jasmonate attenuated LPS-induced decrease of IκBα and increase of p65 and IκBα phosphorylation in HK-2 cell. Conclusion: Methyl jasmonate demonstrated anti-apoptotic and anti-inflammatory effects on LPS-induced HK-2 cell through suppression of NF-κB activation.

scholarly journals Octreotide Alleviates Autophagy by Up-Regulation of MicroRNA-101 in Intestinal Epithelial Cell Line Caco-2

2018 ◽  
Vol 49 (4) ◽  
pp. 1352-1363 ◽  
Author(s):  
Yuling Li ◽  
Su Wang ◽  
Xingjuan Gao ◽  
Ying Zhao ◽  
Yongwei Li ◽  
...  
Keyword(s):  
Tight Junction ◽  
Cell Viability ◽  
Mtor Pathway ◽  
Common Side Effect ◽  
Epithelial Cell Line ◽  
Therapeutic Effects ◽  
Intestinal Epithelial ◽  
Differentiated Cells ◽  
Monolayer Permeability ◽  
Underlying Mechanisms

Background: Intestinal mucositis is a common side-effect after anti-cancer therapy, which may greatly restrict the therapeutic effects. We aimed to explore the functional role of octreotide (OCT) in lipopolysaccharide (LPS)-induced autophagy of human intestinal epithelial cells as well as the underlying mechanisms. Methods: Cell viability and expression of proteins related to autophagy, AMPK and the mTOR pathway in LPS-treated Caco-2 cells were determined by CCK-8 assay and Western blot analysis, respectively. Effects of OCT on LPS-induced alterations as well as miR-101 expression were measured. Then, miR-101 was aberrantly expressed, and whether OCT alleviated LPS-induced autophagy through miR-101 was tested. Next, whether TGF-β-activated kinase 1 (TAK1) was involved in the regulation of miR-101 in LPS-induced autophagy was studied. Effects of OCT on monolayer permeability and tight junction level were analyzed via measuring transepithelial electrical resistance (TEER) and expression of tight junction proteins. Results: LPS reduced cell viability and increased autophagy through activating AMPK and inhibiting the mTOR pathway in Caco-2 cells. OCT alleviated LPS-induced alterations and repressed degradation of autophagosome. Then, we found that OCT affected autophagy through up-regulating miR-101 in LPS-treated cells. Moreover, miR-101-induced inactivation of AMPK and activation of the mTOR pathway in LPS-treated cells were reversed by inhibition of TAK1 phosphorylation. Finally, we found miR-101 was up-regulated in differentiated cells, and OCT protected the monolayer permeability and tight junction level. Conclusion: OCT repressed autophagy through miR-101-mediated inactivation of TAK1, along with inactivation of AMPK and activation of the mTOR pathway in LPS-treated Caco-2 cells.

scholarly journals Methyl jasmonate reduces the inflammation and apoptosis of HK-2 cells induced by LPS by regulating the NF-κB pathway

2021 ◽  
Keyword(s):  
Cell Viability ◽  
Methyl Jasmonate ◽  
Cell Apoptosis ◽  
Cell Model ◽  
Tubular Epithelial Cell ◽  
Cell Protein ◽  
Epithelial Cell Line ◽  
Tnf Α ◽  
Iκbα Phosphorylation ◽  
Anti Inflammatory

Background: Methyl jasmonate is a bioactive oxylipid that participates in the defense-related mechanisms of plants. The anti-inflammatory and anti-oxidative capacities of methyl jasmonate against lipopolysaccharide (LPS) induced arthritis have been widely investigated. However, the role of methyl jasmonate in LPS-induced cell model of tubular-interstitial nephritis (TIN) has not been reported. Methods: LPS (5 µg/mL) was applied to treat human renal tubular epithelial cell line (HK-2) for the establishment of TIN cell model. LPS-induced HK-2 was incubated with 10 or 20 µM methyl jasmonate, cell viability and apoptosis were assessed by MTT and flow cytometry. ELISA and qRT-PCR were performed to determine the levels of interleukin (IL)-1 beta (IL-1β), IL-6, IL-8 and tumor necrosis factor-α (TNF-α). The downstream pathway was investigated by western blot. Results: LPS induced cytotoxicity in HK-2 cell accompanied by decrease of cell viability and increase of cell apoptosis. Methyl jasmonate dosage dependently enhanced the cell viability and reduced cell apoptosis to ameliorate the cytotoxicity. LPS also induced inflammatory response in HK-2 cell with increased IL-1β, IL-6, IL-8 and TNF-α. Methyl jasmonate attenuated LPS-induced inflammation in HK-2 cell. Protein expression of IκBα was down-regulated, p65 and IκBα phosphorylation were up-regulated in LPS-induced HK-2. Methyl jasmonate attenuated LPS-induced decrease of IκBα and increase of p65 and IκBα phosphorylation in HK-2 cell. Conclusion: Methyl jasmonate demonstrated anti-apoptotic and anti-inflammatory effects on LPS-induced HK-2 cell through suppression of NF-κB activation.

scholarly journals The function of antimicrobial peptide MPX on the apoptosis and barrier of IPEC-J2 cells

2021 ◽  
Vol 23 (102) ◽  
pp. 125-129
Author(s):  
Xueqin Zhao
Keyword(s):  
Cell Apoptosis ◽  
Epithelial Cell Line ◽  
Intestinal Epithelial ◽  
Caspase 9 ◽  
E Coli ◽  
Life Threatening ◽  
Porcine Intestinal Epithelial Cell ◽  
Main Components ◽  
Adhesion And Invasion ◽  
Junction Proteins

The porcine intestinal epithelial cell line IPEC-J2 cells, which were isolated from neonatal piglet mid-jejunum, the main components of the intestinal epithelium and play an important role in the intestine. Escherichia coli is an important cause of diarrhea in human and animal. E.coli infections are the leading cause of travelers' diarrhea and a major cause of diarrhea in developing nations, where it can be life-threatening among children. The aim of this study is to explore MPX against E. coli to inhibit IPEC-J2 cells apoptosis and enhance cell barrier. In this study, scanning electron microscopy results found that E. coli infection caused cell apoptosis and destroyed cell membranes of IPEC-J2 cell. MPX effectively alleviated apoptosis of IPEC-J2 cells. The laser confocal results further found that MPX prevented cell apoptosis by inhibiting caspase-3 and caspase-9 activation. In addition, it was found that MPX regulated the expression of tight junction proteins ZO-1, Occludin, and Claudin-1 in IPEC-J2 cells and is closely related to Rac1 by adding a Rac1 inhibitor. The results of adhesion and invasion experiments further found that MPX inhibited bacterial adhesion and invasion through Rac1. The above results indicated that MPX has better function in inhibiting IPEC-J2 cells apoptosis and enhancing cell barrier.

scholarly journals Human breast milk-derived exosomes attenuate cell death in intestinal epithelial cells

2018 ◽  
Vol 24 (5) ◽  
pp. 278-284 ◽  
Author(s):  
Colin Martin ◽  
Mikita Patel ◽  
Sparkle Williams ◽  
Hamish Arora ◽  
Brian Sims
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Breast Milk ◽  
Epithelial Cells ◽  
Protective Effect ◽  
Cell Viability ◽  
Intestinal Epithelial Cells ◽  
Human Breast Milk ◽  
Intestinal Epithelial ◽  
Human Breast

Human breast milk has been shown to reduce the incidence of necrotizing enterocolitis (NEC). Breast milk has many components (immunoglobulins, proteins, fat, and, of recent interest, exosomes), but the specific component that affords protection against NEC is not known. Exosomes are small-nanometer vesicles that are rich in protein, lipid, and microRNA. Here, we hypothesized that human breast milk-derived exosomes can protect intestinal epithelial cells (IECs) from cell death. Human breast milk was collected, separated using ultracentrifugation, and quantified using NanoSight tracking analysis. Purified exosomes were added to IECs that had been treated with varying concentrations of H2O2. Cells were then incubated overnight with the human breast milk-derived exosomes and assessed for cell viability. Western blot analysis showed that both clathrin and CD81 were present in the purified sample. Oxidative stress using H2O2 caused a 50% decrease in cell viability and human breast milk-derived exosomes had a protective effect in IECs. In the presence of H2O2, exosomes had a statistically significant protective effect. The protection seen by human breast milk-derived exosomes was not attenuated by cycloheximide. Thus, human breast milk-derived exosomes allow IECs to be protected from oxidative stress, but the mechanism is still not clear. Exosomes derived from human breast milk are an attractive treatment concept for children with intestinal injury.

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