Protective effects of astaxanthin on lipopolysaccharide-induced inflammation in bovine endometrial epithelial cells†

2019 ◽  
Vol 102 (2) ◽  
pp. 339-347 ◽  
Author(s):  
Fa-Chun Wan ◽  
Chen Zhang ◽  
Qing Jin ◽  
Chen Wei ◽  
Hong-Bo Zhao ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
B Cell Lymphoma ◽  
Resistant Bacteria ◽  
Epithelial Cell Line ◽  
Protective Effects ◽  
Necrosis Factor Alpha ◽  
Antibiotic Resistant ◽  
Injury Treatment ◽  
Endometrial Epithelial Cells

Abstract Astaxanthin (AST), a natural antioxidant carotenoid, has been shown to exert anti-inflammatory effects. However, to our knowledge, no study has specifically addressed the potential protective effects of AST against bovine endometritis. The purpose of this study was to examine whether treatment with AST could protect endometrial epithelial cells against lipopolysaccharide (LPS)-induced inflammatory injury. Treatment of bovine endometrial (BEND) epithelial cell line with AST reduced LPS-induced production of interleukin-6 and tumor necrosis factor-alpha, increased the cellular activity of superoxide dismutase and catalase, decreased the proportion of apoptotic cells, and promoted the production of insulin-like growth factor and epithelial growth factor. The effects of AST were mediated through the downregulation of B-cell lymphoma 2 (Bcl-2) associated X, apoptosis regulator (Bax), and cleaved caspase-3 and through the upregulation of Bcl-2. Moreover, AST significantly increased the expression of the tight junction proteins (TJP) claudin, cadherin-1, and TJP1, which play an essential role in the maintenance of host endometrial defense barrier against pathogen infection. Collectively, these results demonstrated that treatment with AST protected against oxidative stress, prevented cell apoptosis, promoted BEND cells viability, and increased the production of growth factors, in addition to activating the endometrial defense barrier. Therefore, AST is a promising therapeutic agent for the prevention and treatment of endometritis. This finding is of utmost importance in the present times when the excessive use of antibiotics has resulted in the development of antibiotic-resistant bacteria.

scholarly journals Growth factor induced proliferation, migration, and lumen formation of rat endometrial epithelial cells in vitro

2016 ◽  
Vol 62 (3) ◽  
pp. 271-278 ◽  
Author(s):  
Md. Rashedul ISLAM ◽  
Kazuki YAMAGAMI ◽  
Yuka YOSHII ◽  
Nobuhiko YAMAUCHI
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Lumen Formation ◽  
Endometrial Epithelial Cells

Glutamine protects intestinal epithelial cells: role of inducible HSP70

1997 ◽  
Vol 272 (4) ◽  
pp. G879-G884 ◽  
Author(s):  
P. E. Wischmeyer ◽  
M. W. Musch ◽  
M. B. Madonna ◽  
R. Thisted ◽  
E. B. Chang
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Mucosal Healing ◽  
Epithelial Cell Line ◽  
Protective Effects ◽  
Intestinal Epithelial ◽  
Cellular Protection ◽  
Gut Mucosa ◽  
Shock Proteins ◽  
Hsp70 Induction

Glutamine (Gln) protects gut mucosa against injury and promotes mucosal healing. Because the induction of heat shock proteins (HSP) protects cells under conditions of stress, we determined whether Gln conferred protection against stress in an intestinal epithelial cell line through HSP induction. Gln added to IEC-18 cells induces an increase in HSP70, a concentration-dependent effect also seen with mRNA. Two forms of injury, lethal heat (49 degrees C) and oxidant, were used, and viability was determined by 51Cr release. Gln-treated cells were significantly more resistant to injury. Treatment with 6-diazo-5-oxo-L-norleucine (DON), a nonmetabolizable analog of Gln, induced HSP70 and protected cells from injury, but less than Gln. These findings suggest that the effects of Gln on HSP70 induction and cellular protection are mediated by metabolic and nonmetabolic mechanisms. To determine whether HSP induction was central to the action of Gln and DON, quercetin, which blocks HSP induction, was used. Quercetin blocked HSP70 induction and the protective effect of Gln and DON. We conclude that the protective effects of Gln in intestinal epithelial cells are in part mediated by HSP70 induction.

scholarly journals The proliferative effect of cortisol on bovine endometrial epithelial cells

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Junsheng Dong ◽  
Jun Li ◽  
Jianji Li ◽  
Luying Cui ◽  
Xia Meng ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factors ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Signaling Pathways ◽  
Akt Signaling ◽  
Tissue Growth ◽  
Mrna Levels ◽  
Physiological Level ◽  
Endometrial Epithelial Cells

Abstract Background Bovine endometrial epithelial cells (BEECs) undergo regular regeneration after calving. Elevated cortisol concentrations have been reported in postpartum cattle due to various stresses. However, the effects of the physiological level of cortisol on proliferation in BEECs have not been reported. The aim of this study was to investigate whether cortisol can influence the proliferation properties of BEECs and to clarify the possible underlying mechanism. Methods BEECs were treated with different concentrations of cortisol (5, 15 and 30 ng/mL). The mRNA expression of various growth factors was detected by quantitative reverse transcription-polymerase chain reaction (qPCR), progression of the cell cycle in BEECs was measured using flow cytometric analysis, and the activation of the Wnt/β-catenin and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathways was detected with Western blot and immunofluorescence. Results Cortisol treatment resulted in upregulated mRNA levels of vascular endothelial growth factor (VEGF) and connective tissue growth factor (CTGF); however, it had no influence on transforming growth factor-beta1 (TGF-β1). Cortisol (15 ng/mL) accelerated the cell cycle transition from the G0/G1 to the S phase. Cortisol upregulated the expression of β-catenin, c-Myc, and cyclinD1 and promoted the phosphorylation of PI3K and AKT. Conclusions These results demonstrated that cortisol may promote proliferation in BEECs by increasing the expression of some growth factors and activating the Wnt/β-catenin and PI3K/AKT signaling pathways.

scholarly journals Resveratrol Pretreatment Ameliorates p53-Bax Axis and Augments the Survival Biomarker B-Cell Lymphoma 2 Modulated by Paracetamol Overdose in a Rat Model of Acute Liver Injury

Pharmacology ◽  
2019 ◽  
Vol 105 (1-2) ◽  
pp. 39-46 ◽  
Author(s):  
Suliman Al Humayed ◽  
Fahaid Al-Hashem ◽  
Mohamed A. Haidara ◽  
Abbas O. El Karib ◽  
Samaa S. Kamar ◽  
...  
Keyword(s):  
Single Dose ◽  
Liver Injury ◽  
B Cell ◽  
Nitrosative Stress ◽  
Acute Liver Injury ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Paracetamol Overdose ◽  
Protective Effects ◽  
Necrosis Factor Alpha

Background: The potential protective effects of resveratrol (RES) on the modulation of hepatic biomarkers of apoptosis and survival, p53-Bax axis, and B-cell lymphoma 2 (Bcl-2) in an animal model of paracetamol-induced acute liver injury have not been investigated before. Methods: The model group of rats received a single dose of paracetamol (2 g/kg, orally), whereas the protective group of rats were pretreated for 7 days with RES (30 mg/kg, i.p.) before they were given a single dose of paracetamol. All rats were then sacrificed 24-h post paracetamol ingestion. Results: Histology images showed that paracetamol overdose induced acute liver injury, which was substantially protected by RES. Paracetamol significantly (p < 0.05) modulated p53, apoptosis regulator Bax, Bcl-2, tumor necrosis factor-alpha, interleukin-6, inducible nitric oxide synthase, malondialdehyde, superoxide dismutase, glutathione peroxidase, alanine aminotransferase, and aspartate aminotransferase, which were significantly protected by RES. We further demonstrated a significant (p< 0.01) correlation between either p53 or Bcl-2 scoring and the levels of inflammatory, nitrosative stress, and liver injury biomarkers. Conclusion: We demonstrate a substantial protection by RES pretreatment against paracetamol-induced modulation of p53-Bax axis, Bcl-2, and other acute liver injury biomarkers in rats.

scholarly journals Oxytocin Receptor Down-Regulation Is Not Necessary for Reducing Oxytocin-Induced Prostaglandin F2α Accumulation by Interferon-τ in a Bovine Endometrial Epithelial Cell Line

Endocrinology ◽  
2009 ◽  
Vol 150 (2) ◽  
pp. 897-905 ◽  
Author(s):  
Narayanan Krishnaswamy ◽  
Ghislain Danyod ◽  
Pierre Chapdelaine ◽  
Michel A. Fortier
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Line ◽  
Molecular Mechanisms ◽  
Prostaglandin F2α ◽  
Epithelial Cell Line ◽  
Dependent Manner ◽  
Down Regulation ◽  
Endometrial Epithelial Cell ◽  
Endometrial Epithelial Cells

Interferon-τ (IFNτ) is the embryonic signal responsible for pregnancy recognition in ruminants. The primary action of IFNτ is believed to be mediated through inhibition of prostaglandin F2α (PGF2α) released from the endometrial epithelial cells in response to oxytocin (OT). Our working hypothesis was that the antiluteolytic effect of IFNτ also involved modulation of PG production downstream of OT receptor (OTR) and/or cyclooxygenase 2 (COX2). There is currently no OT-sensitive endometrial cell line to study the molecular mechanisms underlying our hypotheses. Therefore, we established an immortalized bovine endometrial epithelial cell line (bEEL) exhibiting OT response. These cells were cytokeratin positive, expressed steroid receptors, and exhibited preferential accumulation of PGF2α over PGE2. The bEEL cells were highly sensitive to OT, showing time- and concentration-dependent increase in COX2 transcript and protein and PGF2α accumulation. Interestingly, IFNτ (20 ng/ml) significantly reduced OT-induced PGF2α accumulation, but surprisingly, the effect was not mediated through down-regulation of either OTR or COX2. Rather, IFNτ up-regulated COX2 in a time- and concentration-dependent manner while decreasing OT-induced PG accumulation. This suggests that COX2 is not a primary target for the antiluteolytic effect of IFNτ. Because IFNτ reduced OT-stimulated PGF2α accumulation within 3 h, the mechanism likely involves a direct interference at the level of the OT signaling or transcription in addition to the down-regulation of OTR observed in vivo. In summary, bEEL cells offer a unique in vitro model for investigating the cellular and molecular mechanisms underlying OT and IFNτ response in relation with luteolysis and recognition of pregnancy in the bovine. Interferon-τ acts as a competitive partial agonist, stimulating basal but inhibiting oxytocin- and phorbol myristate acetate-stimulated prostaglandin F2α production in immortalized bovine endometrial epithelial cells.

Effects of epidermal growth factor and transforming growth factor alpha on the mouse trophoblast outgrowth in vitro

1995 ◽  
Vol 133 (6) ◽  
pp. 741-746 ◽  
Author(s):  
Toshifumi Machida ◽  
Michiyoshi Taga ◽  
Hiroshi Minaguchi
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epithelial Cells ◽  
Conditioned Medium ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Alpha ◽  
Epidermal Growth ◽  
Factor Alpha ◽  
Endometrial Epithelial Cells

Machida T, Taga M, Minaguchi H. Effects of epidermal growth factor and transforming growth factor alpha on the mouse trophoblast outgrowth in vitro. Eur J Endocrinol 1995;133:741–6. ISSN 0804–4643 In order to analyze the involvement of growth factors in the implantation mechanism, we examined the direct effects of epidermal growth factor (EGF) and transforming growth factor alpha (TGF-α) on trophoblast outgrowth of the mouse blastocyst in vitro. ICR mouse blastocysts were cultured for 4 days on a culture plate in medium containing EGF or TGF-α or conditioned medium obtained from cultured endometrial epithelial cells. Blastocysts were also co-cultured with endometrial epithelial cells. The trophoblast outgrowth of these cultured blastocysts was observed daily and the percentage of outgrowing embryos was calculated and analyzed statistically by the chi-squared test. Analysis for the specific binding of 125I-EGF in outgrown trophoblasts was carried out by autoradiography. The coculture (days 3 and 4) and the presence of EGF (10 ng/ml, day 4), TGF-α (1 ng/ml, day 3; 10 ng/ml, days 2 and 3; 50 ng/ml, days 2–4) or conditioned medium (days 3 and 4) significantly stimulated the rate of trophoblast outgrowth. Preincubation of the conditioned medium with monoclonal anti-EGF or anti-TGF-α antibody suppressed the stimulatory effect of the conditioned medium on trophoblast outgrowth. The specific 125I-EGF binding in outgrown trophoblasts was demonstrated by autoradiography. These results suggest that EGF and TGF-α play an important role in the implantation process by directly stimulating trophoblast development. Michiyoshi Taga, Department of Obstetrics and Gynecology, Yokohama City University School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama 236, Japan

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