Reactive oxygen species-quenching and anti-apoptotic effect of polaprezinc on indomethacin-induced small intestinal epithelial cell injury

2010 ◽  
Vol 45 (7) ◽  
pp. 692-702 ◽  
Author(s):  
Tatsushi Omatsu ◽  
Yuji Naito ◽  
Osamu Handa ◽  
Katsura Mizushima ◽  
Natsuko Hayashi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Cell Injury ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Intestinal Epithelial ◽  
Small Intestinal Epithelial Cell ◽  
Apoptotic Effect ◽  
Small Intestinal

Prostanoids mediate the protective effect of trefoil factor 3 in oxidant-induced intestinal epithelial cell injury: role of cyclooxygenase-2

2000 ◽  
Vol 113 (12) ◽  
pp. 2149-2155
Author(s):  
X.D. Tan ◽  
Y.H. Chen ◽  
Q.P. Liu ◽  
F. Gonzalez-Crussi ◽  
X.L. Liu
Keyword(s):  
Reactive Oxygen Species ◽  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Cell Injury ◽  
Cyclooxygenase 2 ◽  
Prostaglandin E ◽  
Oxygen Species ◽  
Intestinal Epithelial ◽  
Trefoil Factor ◽  
Trefoil Factor 3

Trefoil factors are small peptides found in several mammalian tissues including gut, respiratory tract and brain. Their physiological function is not well understood. Among them, trefoil factor 3 (intestinal trefoil factor) is known to be cytoprotective in the gut. However, the molecular mechanism and secondary mediators of trefoil factor 3 action are not known. In the present study, we examined whether the cyclooxygenase pathway is involved in trefoil factor 3 action. We showed that trefoil factor 3 significantly induces the production of prostaglandin E(2) and prostaglandin I(2) in IEC-18 cells (an intestinal epithelial cell line) in a dose dependent manner. Western blot and immunohistochemistry revealed that trefoil factor 3 (2.5 microM) up-regulates the expression of cyclooxygenase-2 but not cyclooxygenase-1 in IEC-18 cells. Treating cells with trefoil factor 3 (10 microM) significantly attenuated reactive oxygen species-induced IEC-18 cell injury. This effect is blocked by NS-398 (10 microM), a selective cyclooxygenase-2 inhibitor. Moreover, we demonstrated that exogenously administered carbacyclin (1 microM, a stable analogue of prostaglandin I(2)) and/or prostaglandin E(2) (1 microM) caused a significant reduction of reactive oxygen species-induced cell injury, mimicking the effect of trefoil factor 3. In summary, our results indicate that trefoil factor 3 activates cyclooxygenase-2 in intestinal epithelium to produce prostaglandin I(2) and prostaglandin E(2), which function as survival factors and mediate the cytoprotective action of trefoil factor 3 against oxidant injury.

Lipid Composition of Liposomal Membrane Largely Affects Its Transport and Uptake through Small Intestinal Epithelial Cell Models

Lipids ◽  
2020 ◽  
Vol 55 (6) ◽  
pp. 671-682 ◽  
Author(s):  
Keisuke Konishi ◽  
Lei Du ◽  
Grégory Francius ◽  
Michel Linder ◽  
Tomoaki Sugawara ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Lipid Composition ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Cell Models ◽  
Liposomal Membrane ◽  
Small Intestinal Epithelial Cell ◽  
Small Intestinal

Oxygen free radical injury of IEC-18 small intestinal epithelial cell monolayers

1991 ◽  
Vol 100 (6) ◽  
pp. 1533-1543 ◽  
Author(s):  
Thomas Y. Ma ◽  
Daniel Hollander ◽  
Doug Freeman ◽  
Thang Nguyen ◽  
Pavel Krugliak
Keyword(s):  
Free Radical ◽  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Oxygen Free Radical ◽  
Intestinal Epithelial ◽  
Cell Monolayers ◽  
Small Intestinal Epithelial Cell ◽  
Epithelial Cell Monolayers ◽  
Small Intestinal

scholarly journals Transport and uptake effects of marine complex lipid liposomes in small intestinal epithelial cell models

2016 ◽  
Vol 7 (4) ◽  
pp. 1904-1914 ◽  
Author(s):  
Lei Du ◽  
Yu-Hong Yang ◽  
Jie Xu ◽  
Yu-Ming Wang ◽  
Chang-Hu Xue ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Cell Monolayer ◽  
Intestinal Epithelial ◽  
Cell Models ◽  
M Cell ◽  
Small Intestinal Epithelial Cell ◽  
Complex Lipid ◽  
Small Intestinal ◽  
Lipid Liposomes

Transport and uptake effects of marine complex lipid liposomes in Caco-2 and M cell monolayer models.

scholarly journals Toxoplasma gondii Induces Apoptosis via Endoplasmic Reticulum Stress-Derived Mitochondrial Pathway in Human Small Intestinal Epithelial Cell-Line

2021 ◽  
Vol 59 (6) ◽  
pp. 573-583
Author(s):  
Hao Wang ◽  
Chunchao Li ◽  
Wei Ye ◽  
Zhaobin Pan ◽  
Jinhui Sun ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Epithelial Cell ◽  
Er Stress ◽  
Mitochondrial Dysfunction ◽  
Host Cell ◽  
Intestinal Epithelial Cell ◽  
Host Cells ◽  
Intestinal Epithelial ◽  
Small Intestinal Epithelial Cell ◽  
Small Intestinal

Toxoplasma gondii, an intracellular protozoan parasite that infects one-third of the world’s population, has been reported to hijack host cell apoptotic machinery and promote either an anti- or proapoptotic program depending on the parasite virulence and load and the host cell type. However, little is known about the regulation of human FHs 74 small intestinal epithelial cell viability in response to T. gondii infection. Here we show that T. gondii RH strain tachyzoite infection or ESP treatment of FHs 74 Int cells induced apoptosis, mitochondrial dysfunction and ER stress in host cells. Pretreatment with 4-PBA inhibited the expression or activation of key molecules involved in ER stress. In addition, both T. gondii and ESP challenge-induced mitochondrial dysfunction and cell death were dramatically suppressed in 4-PBA pretreated cells. Our study indicates that T. gondii infection induced ER stress in FHs 74 Int cells, which induced mitochondrial dysfunction followed by apoptosis. This may constitute a potential molecular mechanism responsible for the foodborne parasitic disease caused by T. gondii.

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