scholarly journals Chrysin Modulates Genes Related to Inflammation, Tissue Remodeling, and Cell Proliferation in the Gastric Ulcer Healing

2020 ◽  
Vol 21 (3) ◽  
pp. 760 ◽  
Author(s):  
Felipe Leonardo Fagundes ◽  
Graziele de Morais Piffer ◽  
Larissa Lucena Périco ◽  
Vinicius Peixoto Rodrigues ◽  
Clélia Akiko Hiruma-Lima ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Acetic Acid ◽  
Gastric Ulcer ◽  
Gastric Mucosa ◽  
Caspase 3 ◽  
Ischemia Reperfusion ◽  
Absolute Ethanol ◽  
Gastric Ulcers ◽  
Healing Effect ◽  
Cox 2

Chrysin exhibits anti-inflammatory and antioxidant activities. Here, the gastroprotective effect of chrysin was investigated in mouse models of gastric ulcer induced by absolute ethanol, acetic acid, and ischemia-reperfusion injury. The gastric-healing effect was evaluated at 7 and 14 days after treatment; the mechanism of action was verified using the expression of metalloproteinase 2 (MMP-2) and 9 (MMP-9), caspase-3, cyclooxygenase 1 (COX-1) and 2 (COX-2), epidermal growth factor (EGF), and interleukin-10. Chrysin (10 mg/kg) inhibited macroscopic lesions and increased catalase activity in the mouse model established using absolute ethanol. It ameliorated the gastric ulcer caused by acetic acid by improving the expression of inflammatory genes such as COX-2, inhibiting negative remodeling promoted by MMP-9, increasing cell proliferation effect via EGF, and reducing cellular apoptosis by modulating caspase-3. A faster healing effect was evident in the first 7 days of treatment compared to 14 days of treatment, indicating the pharmacological potential of chrysin. Overall, these results demonstrate the potent effect of chrysin in the gastrointestinal tract and elucidate the genes involved in the healing of gastric ulcers. Moreover, an increase in the levels of gastric mucosa defensive factors is involved in the activity of chrysin in the gastric mucosa.

Angiogenesis, cell proliferation and apoptosis in gastric ulcer healing. Effect of a selective cox-2 inhibitor

2004 ◽  
Vol 505 (1-3) ◽  
pp. 187-194 ◽  
Author(s):  
Susana Sánchez-Fidalgo ◽  
Inés Martín-Lacave ◽  
Matilde Illanes ◽  
Virginia Motilva
Keyword(s):  
Cell Proliferation ◽  
Gastric Ulcer ◽  
Ulcer Healing ◽  
Gastric Ulcer Healing ◽  
Healing Effect ◽  
Proliferation And Apoptosis ◽  
Cox 2

scholarly journals Immunohistochemical Studies of Age-Related Changes in Cell Proliferation and Angiogenesis during the Healing of Acetic Acid-Induced Gastric Ulcers in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
A. Folorunsho Ajayi ◽  
S. Babafemi Olaleye
Keyword(s):  
Cell Proliferation ◽  
Acetic Acid ◽  
Gastric Ulcer ◽  
Factor Viii ◽  
Ulcer Healing ◽  
Gastric Ulcers ◽  
Gastric Injury ◽  
Tissue Samples ◽  
Age Related ◽  
Male Wistar Rats

Cell proliferation and angiogenesis are of utmost importance for healing to take place. The KI67 and EGFR proteins are markers of cell proliferation, while CD31 and factor VIII are markers of angiogenesis. To elucidate the mechanism responsible for delayed healing of the gastric injury in old age, we analyzed the expression of these markers in rats of different months during the healing of an acetic acid-induced gastric ulcer. Male Wistar rats (aged 3, 6, 12, and 18 months) divided into four groups, according to their ages, formed the experimental animals. Stomach tissue samples were collected on days 3, 7, 14, and 21 after induction for assessment of ulcer healing. The area of gastric mucosa healed was inversely proportional to age. The expression of markers of proliferation (KI67 and EGFR) and angiogenesis (factor VIII and CD31) decreased significantly (p<0.05) in older rats when compared with younger ones (3 months > six months > 12 months > 18 months) on days 7, 14, and 21 after induction of gastric ulcer. This study revealed that the slower gastric ulcer healing rate in older rats might be due to reduced epithelial cell proliferation and angiogenic activities.

scholarly journals Protective Effect of Ocotillol, the Derivate of Ocotillol-Type Saponins in Panax Genus, against Acetic Acid-Induced Gastric Ulcer in Rats Based on Untargeted Metabolomics

2020 ◽  
Vol 21 (7) ◽  
pp. 2577 ◽  
Author(s):  
Cuizhu Wang ◽  
Yuze Yuan ◽  
He Pan ◽  
Alan Chen-Yu Hsu ◽  
Jinluan Chen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Acetic Acid ◽  
Gastric Ulcer ◽  
Growth Factor ◽  
Gastric Mucosa ◽  
Epidermal Growth Factor ◽  
Serum Levels ◽  
Gastroprotective Effect ◽  
Epidermal Growth ◽  
Oxide Synthase

Gastric ulcer (GU), a prevalent digestive disease, has a high incidence and is seriously harmful to human health. Finding a natural drug with a gastroprotective effect is needed. Ocotillol, the derivate of ocotillol-type saponins in the Panax genus, possesses good anti-inflammatory activity. The study aimed to investigate the gastroprotective effect of ocotillol on acetic acid-induced GU rats. The serum levels of endothelin-1 (ET-1) and nitric oxide (NO), the gastric mucosa levels of epidermal growth factor, superoxide dismutase and NO were assessed. Hematoxylin and eosin staining of gastric mucosa for pathological changes and immunohistochemical staining of ET-1, epidermal growth factor receptors and inducible nitric oxide synthase were evaluated. A UPLC-QTOF-MS-based serum metabolomics approach was applied to explore the latent mechanism. A total of 21 potential metabolites involved in 7 metabolic pathways were identified. The study helps us to understand the pathogenesis of GU and to provide a potential natural anti-ulcer agent.

scholarly journals A preliminary study of the anti-inflammatory and anti-apoptotic effects of crocin against gastric ischemia-reperfusion injury in rats

2015 ◽  
Vol 51 (3) ◽  
pp. 637-642 ◽  
Author(s):  
Seyyed Ali Mard ◽  
Zahra Nikraftar ◽  
Yaghoob Farbood ◽  
Esrafil Mansouri
Keyword(s):  
Gastric Mucosa ◽  
Protein Expression ◽  
Protective Effect ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Celiac Artery ◽  
Male Rats ◽  
Gastric Mucosal Lesions ◽  
Inflammatory Protein

The aim of the present study was to investigate the protective effect of crocin on gastric mucosal lesions caused by ischemia-reperfusion (I/R) injury in rats. Thirty-two male rats were randomly divided into sham, I/R, I/R + crocin pretreatment and crocin alone groups. To induce I/R lesions, the celiac artery was clamped for 30 min, and the clamp was then removed to allow reperfusion for 3 h. Crocin-pretreated rats received crocin (15 mg/kg, i.p.) 30 min prior to the induction of I/R injury. Samples of gastric mucosa were collected to quantify the protein expression of caspase-3, an apoptotic factor, and inducible nitric oxide synthase (iNOS), a pro-inflammatory protein, by Western blot. Pretreatment with crocin decreased the total area of gastric lesions and decreased the protein expression levels of caspase-3 and iNOS induced by I/R injury. Our findings showed a protective effect of crocin in gastric mucosa against I/R injury. This effect of crocin was mainly mediated by reducing the protein expression of iNOS and caspase-3.

A STUDY ON THE RELATIONSHIP BETWEEN HELICOBACTER PYLORI AND TRACE ELEMENTS IN GASTRIC MUCOSA

2006 ◽  
Vol 16 (01n02) ◽  
pp. 55-68
Author(s):  
T. FUKUDA ◽  
S. SAKURAI ◽  
M. KUDO
Keyword(s):  
Helicobacter Pylori ◽  
Trace Elements ◽  
Gastric Ulcer ◽  
Gastric Mucosa ◽  
Gastric Ulcers ◽  
Control Group ◽  
Human Gastric Mucosa ◽  
H2 Receptor Antagonist ◽  
Zinc Levels ◽  
The Relationship

H2 receptor antagonist (H2RA) and proton pump inhibitor(PPI) are often used to treat gastric ulcers, in addition to the zinc-L-carcino-complex which is commonly adopted for such therapies. However, there have been no previous reports detailing the levels and distribution of zinc in human gastric mucosa. The aim of our current study is to clarify the relationship between Helicobacter pylori infection and trace elements such as zinc in gastric mucosa using particle induced X-ray emission (PIXE). Forty gastric ulcer patients were chosen as subjects of this study and divided into two groups. One is a new ulcer patients group(twenty nine cases). And the other, eleven of these patients had been prescribed zinc-L-carcino-complex (polapreZinc®), at a dose of 150mg/day for periods ranging from 16 to 20 weeks. The zinc levels in the gastric ulcer group were found to be significantly less than those of the control group and the concentrations of zinc in gastric mucosa were observed to increase following the administration of treatments containing this element.

scholarly journals Antioxidant Action of Mangrove Polyphenols against Gastric Damage Induced by Absolute Ethanol and Ischemia-Reperfusion in the Rat

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Felipe Meira de-Faria ◽  
Ana Cristina Alves Almeida ◽  
Anderson Luiz-Ferreira ◽  
Christiane Takayama ◽  
Ricardo José Dunder ◽  
...  
Keyword(s):  
Gastric Ulcer ◽  
Ischemia Reperfusion ◽  
Antioxidant Properties ◽  
Lipid Peroxides ◽  
Antioxidant Property ◽  
Absolute Ethanol ◽  
Gastric Injury ◽  
Bark Extract ◽  
Enzymatic Assays ◽  
Red Mangrove

Rhizophora mangle, the red mangrove, has long been known as a traditional medicine. Its bark has been used as astringent, antiseptic, hemostatic, with antifungic and antiulcerogenic properties. In this paper, we aimed to evaluate the antioxidant properties of a buthanolic fraction of theR. manglebark extract (RM) against experimental gastric ulcer in rats. Unib-Wh rats received pretreatment ofR. mangleafter the induction of gastric injury with absolute ethanol and ischemia-reperfusion. Gastric tissues from both methods were prepared to the enzymatic assays, the levels of sulfhydril compounds (GSH), lipid peroxides (LPO), and the activities of glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD) and myeloperoxidase (MPO) were measured. The RM protected the gastric mucosa in both methods used, ethanol-induced gastric ulcer and ischemia-reperfusion, probably, by modulating the activities of the enzymes SOD, GPx, and GR and increasing or maintaining the levels of GSH; in adittion, LPO levels were reduced. The results suggest that the RM antioxidant activity leads to tissue protection; thus one of the antiulcer mechanisms present on the pharmacological effects ofR. mangleis the antioxidant property.

COX-2 protects gastric mucosa against ischemia-reperfusion injuries through down-regulation of the expression of ICAM-1 in mice

2001 ◽  
Vol 120 (5) ◽  
pp. A151
Author(s):  
Tetsuro Hiratsuka ◽  
Seiji Futagami ◽  
Atsusi Tatsuguchi ◽  
Ken Wada ◽  
Tomonori M. Akamatsu ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Ischemia Reperfusion ◽  
Down Regulation ◽  
Cox 2

scholarly journals Long noncoding RNA-MEG3 contributes to myocardial ischemia–reperfusion injury through suppression of miR-7-5p expression

2019 ◽  
Vol 39 (8) ◽  
Author(s):  
Liyuan Zou ◽  
Xiaokun Ma ◽  
Shuo Lin ◽  
Bingyuan Wu ◽  
Yang Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Cell Model ◽  
Ischemia Reperfusion ◽  
Luciferase Reporter

Abstract Long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) plays an important role in protection of ischemia–reperfusion (I/R) injury in brain and liver. However, role of MEG3 in myocardial I/R injury remains unclear. Here, the role of MEG3 in protection of myocardial I/R injury and its association with microRNA-7-5p (miR-7-5p) was investigated using rat cardiac I/R model and myocardial I/R cell model. Our results showed that MEG3 was significantly up-regulated and miR-7-5p was significantly down-regulated after I/R. Following I/R, the levels of intact PARP and intact caspase-3 were reduced, while the cleaved fragments of PARP and caspase-3 were increased. TUNEL assay showed an increase in cardiomyocyte apoptosis after I/R. The levels of I/R-induced creatine kinase (CK) and lactate dehydrogenase (LDH) were inhibited by knockdown of MEG3 (siMEG3). SiMEG3 increased cell proliferation and inhibited cell apoptosis after I/R. In contrast, overexpression of MEG3 increased the I/R-induced CK and LDH activities and cell apoptosis and decreased cell proliferation. The dual-luciferase reporter system showed a direct binding of MEG3 to miR-7-5p. The level of miR-7-5p was negatively associated with the change in levels of MEG3 in H9c2 cells. The levels of intact RARP1 and caspase-3 were significantly increased by knockdown of MEG3. Co-transfection of miR-7-5p inhibitor with siMEG3 activates CK and LDH, significantly decreased cell proliferation, increased cell apoptosis, and decreased intact poly(ADP-ribose) polymerase 1 (PARP1) and caspase-3. In summary, down-regulation of MEG3 protects myocardial cells against I/R-induced apoptosis through miR-7-5p/PARP1 pathway, which might provide a new therapeutic target for treatment of myocardial I/R injury.

COX-2 protects gastric mucosa against ischemia-reperfusion injuries through down-regulation of the expression of ICAM-1 in mice

2001 ◽  
Vol 120 (5) ◽  
pp. A151-A151
Author(s):  
T HIRATSUKA ◽  
S FUTAGAMI ◽  
A TATSUGUCHI ◽  
K WADA ◽  
T AKAMATSU ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Ischemia Reperfusion ◽  
Down Regulation ◽  
Cox 2

scholarly journals Neuroprotective Effect of DAHP via Antiapoptosis in Cerebral Ischemia

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Yanhua Qin ◽  
Weiming Hu ◽  
Yang Yang ◽  
Zhiying Hu ◽  
Weiyun Li ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Brain Injury ◽  
Cerebral Ischemia ◽  
Caspase 3 ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Tunel Staining ◽  
Cox 2

Aberrant production of nitric oxide following inducible nitric oxide synthase (iNOS) expression has been implicated in cell death and contributes to ischemic brain injury. Tetrahydrobiopterin (BH4) is an essential cofactor of NOS activity. Herein, we evaluated antiapoptotic and anti-inflammatory effects of diamino-6-hydroxypyrimidine (DAHP), a guanosine 5′-triphosphate cyclohydrolase 1 (GTPCH1) inhibitor on focal cerebral ischemia-reperfusion injury by middle cerebral artery occlusion and reperfusion (MCAO) and investigated the underlying mechanism. Sprague-Dawley rats were divided into five groups. Experimental groups were subjected to 1.5 h transient MCAO. T2-weighted imaging was performed to evaluate brain edema lesions in the stroke rats. Infarct volume was estimated by 2,3,5-triphenyltetrazolium chloride (TTC) staining after 24 h reperfusion. Western blotting and immunohistochemistry were performed to detect iNOS, caspase-3, Bcl-2, COX-2, and TNF-α protein expressions. Apoptosis was determined by TUNEL staining. T2 hyperintensity changes were observed in primary ischemic region. DAHP pretreatment significantly suppressed iNOS overexpression, caspase-3, and TNF-α. There was also attenuation of neuronal apoptosis with decrement in proteins Bcl-2 and COX-2 expressions. On the basis of our results, we hypothesize DAHP to have a neuroprotective function against focal cerebral ischemia and might attenuate brain injury by decreasing reactive oxygen species (ROS) production, subsequently inhibiting apoptosis.

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