scholarly journals Protective effect of polydatin on radiation-induced injury of intestinal epithelial and endothelial cells

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Li Li ◽  
Ke Zhang ◽  
Ji Zhang ◽  
Ya-Nan Zeng ◽  
Feng Lai ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Small Intestine ◽  
Vascular Endothelial Cells ◽  
Tissue Sample ◽  
Proliferative Potential ◽  
Vascular Endothelial ◽  
Intestinal Epithelial ◽  
Intestinal Villi ◽  
Radiation Induced ◽  
Hematoxylin And Eosin

This study aimed to examine the radioprotective effect of polydatin (PD) on crypt and endothelial cells of the small intestines of C57BL/6 mice that received abdominal irradiation (IR). Mice were treated with 6 MV X-ray (20 Gy) abdominal IR at a dose rate of 200 cGy/min. Thirty minutes before or after IR, mice were intraperitoneally injected with PD. The rate of survival of the mice at 30 days after IR was determined. The duodenum (upper small intestine), jejunum (middle small intestine), and ileum (lower small intestine) were collected and subjected to hematoxylin and eosin staining. Tissue sample sections were analyzed through light microscopy, and the lengths of at least 20 intestinal villi were measured in each group; the average number of crypts was obtained from 10 intestinal samples in each group. Microvessel density was assessed using CD31-positive (brown) vascular endothelial cells/cell clusters. FHs74Int cell proliferation was measured using the CCK-8 assay. PD administration (25 mg/kg) before IR was the most effective in prolonging the survival of C57BL/6 mice. PD reduced radiation-induced injury of intestinal villi, prevented loss of crypts, increased intestinal crypt growth, protected against IR-induced intestinal injury, and enhanced the proliferative potential and reduced the apoptosis of FHs74Int cells after IR. Moreover, PD increased small intestinal MVD and reduced the apoptosis of intestinal microvascular endothelial cells in mice after IR. Therefore, PD was found to be able to protect the two types of cells from radiation damage and to thus alleviate radiation-induced injury of small intestine.

scholarly journals Stromal Cell-Derived Factor 1 Protects Brain Vascular Endothelial Cells from Radiation-Induced Brain Damage

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1230 ◽  
Author(s):  
Heo ◽  
Kim ◽  
Woo ◽  
Kim ◽  
Choi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Stromal Cell ◽  
Radiation Treatment ◽  
Vascular Endothelial Cells ◽  
Critical Role ◽  
Vascular Endothelial ◽  
Brain Endothelial Cells ◽  
Endothelial Cell Function ◽  
Radiation Induced ◽  
Stromal Cell Derived Factor

Stromal cell-derived factor 1 (SDF-1) and its main receptor, CXC chemokine receptor 4 (CXCR4), play a critical role in endothelial cell function regulation during cardiogenesis, angiogenesis, and reendothelialization after injury. The expression of CXCR4 and SDF-1 in brain endothelial cells decreases due to ionizing radiation treatment and aging. SDF-1 protein treatment in the senescent and radiation-damaged cells reduced several senescence phenotypes, such as decreased cell proliferation, upregulated p53 and p21 expression, and increased senescence-associated beta-galactosidase (SA-β-gal) activity, through CXCR4-dependent signaling. By inhibiting extracellular signal-regulated kinase (ERK) and signal transducer and activator of transcription protein 3 (STAT3), we confirmed that activation of both is important in recovery by SDF-1-related mechanisms. A CXCR4 agonist, ATI2341, protected brain endothelial cells from radiation-induced damage. In irradiation-damaged tissue, ATI2341 treatment inhibited cell death in the villi of the small intestine and decreased SA-β-gal activity in arterial tissue. An ischemic injury experiment revealed no decrease in blood flow by irradiation in ATI2341-administrated mice. ATI2341 treatment specifically affected CXCR4 action in mouse brain vessels and partially restored normal cognitive ability in irradiated mice. These results demonstrate that SDF-1 and ATI2341 may offer potential therapeutic approaches to recover tissues damaged during chemotherapy or radiotherapy, particularly by protecting vascular endothelial cells.

scholarly journals Black soybean seed coat polyphenols promote nitric oxide production in the aorta through the Akt/eNOS pathway

2020 ◽  
Vol 10 (8) ◽  
pp. 330
Author(s):  
Chiaki Domae ◽  
Hitoshi Ashida ◽  
Yoko Yamashita
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Seed Coat ◽  
Vascular Endothelial Cells ◽  
Soybean Seed ◽  
No Production ◽  
Vascular Endothelial ◽  
Intestinal Epithelial ◽  
Black Soybean ◽  
Soybean Seed Coat

Background: Black soybean seed coat contains an abundance of flavan-3-ols and possesses various bioregulatory functions. Nitric oxide (NO) is produced by endothelial nitric oxide synthase (eNOS) in vascular endothelial cells and regulates vascular function through vasodilation and the inhibition of platelet aggregation in blood vessels. It has been reported that flavan-3-ols increase NO production, but many previous reports used a high concentration of flavan-3-ols. In the present study, we investigated the effect of flavan-3-ol-rich black soybean seed coat extract (BE) on NO production at a lower concentration that is close to the concentration after permeation through the monolayer of Caco-2 cells.Methods: Human umbilical vein endothelial cells (HUVEC) were incubated with BE, and then NO production in the medium and eNOS phosphorylation in the cells were examined. Intestinal epithelial Caco-2 cells on the upper side of a transwell filter were co-cultured with HUVEC on the basolateral compartment of the transwell apparatus. BE was added from the upper side, and the basolateral medium was collected to measure the concentration of NO and the content of flavan-3-ols. Furthermore, HUVEC were incubated with each flavan-3-ol in order to individuate the most effective compound in BE.Results: BE significantly increased NO production in the medium of HUVEC. When polyphenols in BE were removed from the basolateral medium by ethyl acetate extraction, increased NO production from HUVEC was not observed. Additionally, BE increased phosphorylation of eNOS and Akt in HUVEC. A portion of flavan-3-ols in BE had permeated through intestinal epithelial cells. Among the flavan-3-ols that had permeated, procyanidin C1 had the strongest effect on NO production in HUVEC at the concentration that had permeated the monolayer of Caco-2 cells. Procyanidin C1 (0.05 µM) also induced phosphorylation of eNOS and Akt in HUVEC without affecting the cAMP level. Conclusion: A portion of flavan-3-ols in BE directly promoted NO production through the Akt/eNOS pathway in vascular endothelial cells. These findings suggest that flavan-3-ols in the black soybean seed coat may contribute to improve the vascular function.Keywords: Black soybean seed coat polyphenols; NO; eNOS; Akt; vascular endothelial cells

scholarly journals Clostridium perfringens type C necrotic enteritis in pigs: diagnosis, pathogenesis, and prevention

2020 ◽  
Vol 32 (2) ◽  
pp. 203-212 ◽  
Author(s):  
Horst Posthaus ◽  
Sonja Kittl ◽  
Basma Tarek ◽  
Julia Bruggisser
Keyword(s):  
Small Intestine ◽  
Clostridium Perfringens ◽  
Vascular Endothelial Cells ◽  
Necrotic Enteritis ◽  
Vascular Endothelial ◽  
Intestinal Epithelial ◽  
Long Time ◽  
Type C ◽  
Mucosal Necrosis ◽  
Beta Toxin

Clostridium perfringens type C causes severe and lethal necrotic enteritis (NE) in newborn piglets. NE is diagnosed through a combination of pathology and bacteriologic investigations. The hallmark lesion of NE is deep, segmental mucosal necrosis with marked hemorrhage of the small intestine. C. perfringens can be isolated from intestinal samples in acute cases but it is more challenging to identify pathogenic strains in subacute-to-chronic cases. Toxinotyping or genotyping is required to differentiate C. perfringens type C from commensal type A strains. Recent research has extended our knowledge about the pathogenesis of the disease, although important aspects remain to be determined. The pathogenesis involves rapid overgrowth of C. perfringens type C in the small intestine, inhibition of beta-toxin (CPB) degradation by trypsin inhibitors in the colostrum of sows, and most likely initial damage to the small intestinal epithelial barrier. CPB itself acts primarily on vascular endothelial cells in the mucosa and can also inhibit platelet function. Prevention of the disease is achieved by immunization of pregnant sows with C. perfringens type C toxoid vaccines, combined with proper sanitation on farms. For the implementation of prevention strategies, it is important to differentiate between disease-free and pathogen-free status of a herd. The latter is more challenging to maintain, given that C. perfringens type C can persist for a long time in the environment and in the intestinal tract of adult animals and thus can be distributed via clinically and bacteriologically inapparent carrier animals.

scholarly journals Celecoxib Alleviates Radiation-Induced Brain Injury in Rats by Maintaining the Integrity of Blood-Brain Barrier

Dose-Response ◽  
2021 ◽  
Vol 19 (2) ◽  
pp. 155932582110243
Author(s):  
Xiaoting Xu ◽  
Hao Huang ◽  
Yu Tu ◽  
Jiaxing Sun ◽  
Yaozu Xiong ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Brain Injury ◽  
Protective Effect ◽  
Blood Brain Barrier ◽  
Vascular Endothelial Cells ◽  
Brain Barrier ◽  
Vascular Endothelial ◽  
Blood Brain ◽  
Radiation Induced ◽  
Cox 2

The underlying mechanisms of radiation-induced brain injury are poorly understood, although COX-2 inhibitors have been shown to reduce brain injury after irradiation. In the present study, the effect of celecoxib (a selective COX-2 inhibitor) pretreatment on radiation-induced injury to rat brain was studied by means of histopathological staining, evaluation of integrity of blood-brain barrier and detection of the expressions of inflammation-associated genes. The protective effect of celecoxib on human brain microvascular endothelial cells (HBMECs) against irradiation was examined and the potential mechanisms were explored. Colony formation assay and apoptosis assay were undertaken to evaluate the effect of celecoxib on the radiosensitivity of the HBMECs. ELISA was used to measure 6-keto-prostaglandin F1α (6-keto-PGF1α) and thromboxane B2 (TXB2) secretion. Western blot was employed to examine apoptosis-related proteins expressions. It was found that celecoxib protected rat from radiation-induced brain injury by maintaining the integrity of the blood-brain barrier and reducing inflammation in rat brain tissues. In addition, celecoxib showed a significant protective effect on HBMECs against irradiation, which involves inhibited apoptosis and decreased TXB2/6-keto-PGF1α ratio in brain vascular endothelial cells. In conclusion, celecoxib could alleviate radiation-induced brain injury in rats, which may be partially due to the protective effect on brain vascular endothelial cells from radiation-induced apoptosis.

Roles of ROS and PKC-βII in ionizing radiation-induced eNOS activation in human vascular endothelial cells

2015 ◽  
Vol 70 ◽  
pp. 55-65 ◽  
Author(s):  
Kimimasa Sakata ◽  
Takashi Kondo ◽  
Natsumi Mizuno ◽  
Miki Shoji ◽  
Hironobu Yasui ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Ionizing Radiation ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Radiation Induced

scholarly journals Enhanced Adhesion of Early Endothelial Progenitor Cells to Radiation-induced Senescence-like Vascular Endothelial Cells in vitro

2009 ◽  
Vol 50 (5) ◽  
pp. 469-475 ◽  
Author(s):  
Nuttawut SERMSATHANASAWADI ◽  
Hideto ISHII ◽  
Kaori IGARASHI ◽  
Masahiko MIURA ◽  
Masayuki YOSHIDA ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Endothelial Progenitor ◽  
Radiation Induced

Radiation-induced senescence-like phenotype in proliferating and plateau-phase vascular endothelial cells

2007 ◽  
Vol 313 (15) ◽  
pp. 3326-3336 ◽  
Author(s):  
Kaori Igarashi ◽  
Ippei Sakimoto ◽  
Keiko Kataoka ◽  
Keisuke Ohta ◽  
Masahiko Miura
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Plateau Phase ◽  
Radiation Induced

Hypoxia-induced proliferation of tissue-resident endothelial progenitor cells in the lung

2015 ◽  
Vol 308 (8) ◽  
pp. L746-L758 ◽  
Author(s):  
Rintaro Nishimura ◽  
Tetsu Nishiwaki ◽  
Takeshi Kawasaki ◽  
Ayumi Sekine ◽  
Rika Suda ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Fluorescent Protein ◽  
Vascular Endothelial Cells ◽  
Vascular Wall ◽  
Proliferative Potential ◽  
Vascular Endothelial ◽  
Endothelial Progenitor ◽  
Hypoxic Conditions

Exposure to hypoxia induces changes in the structure and functional phenotypes of the cells composing the pulmonary vascular wall from larger to most peripheral vessels. Endothelial progenitor cells (EPCs) may be involved in vascular endothelial repair. Resident EPCs with a high proliferative potential are found in the pulmonary microcirculation. However, their potential location, identification, and functional role have not been clearly established. We investigated whether resident EPCs or bone marrow (BM)-derived EPCs play a major role in hypoxic response of pulmonary vascular endothelial cells (PVECs). Mice were exposed to hypoxia. The number of PVECs transiently decreased followed by an increase in hypoxic animals. Under hypoxic conditions for 1 wk, prominent bromodeoxyuridine incorporation was detected in PVECs. Some Ki67-positive cells were detected among PVECs after 1 wk under hypoxic conditions, especially in the capillaries. To clarify the origin of proliferating endothelial cells, we used BM chimeric mice expressing green fluorescent protein (GFP). The percentage of GFP-positive PVECs was low and constant during hypoxia in BM-transplanted mice, suggesting little engraftment of BM-derived cells in lungs under hypoxia. Proliferating PVECs in hypoxic animals showed increased expression of CD34, suggesting hypoxia-induced gene expression and cell surface antigen of EPC or stem/progenitor cells markers. Isolated PVECs from hypoxic mice showed colony- and tube-forming capacity. The present study indicated that hypoxia could induce proliferation of PVECs, and the origin of these cells might be tissue-resident EPCs.

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