Stimulation of colonic mucosal growth associated with oxidized redox status in rats

2007 ◽  
Vol 292 (3) ◽  
pp. R1081-R1091 ◽  
Author(s):  
Junqiang Tian ◽  
Naohiro Washizawa ◽  
Li H. Gu ◽  
Marc S. Levin ◽  
Lihua Wang ◽  
...  
Keyword(s):  
Small Bowel ◽  
Animal Models ◽  
Redox Status ◽  
Crypt Cell ◽  
Brdu Incorporation ◽  
Intestinal Cell ◽  
Dependent Manner ◽  
Colonic Crypt ◽  
Crypt Depth ◽  
Mucosal Growth

Limited data in animal models suggest that colonic mucosa undergoes adaptive growth following massive small bowel resection (SBR). In vitro data suggest that intestinal cell growth is regulated by reactive oxygen species and redox couples [e.g., glutathione (GSH)/glutathione disulfide (GSSG) and cysteine (Cys)/cystine (CySS) redox]. We investigated the effects of SBR and alterations in redox on colonic growth indexes in rats after either small bowel transection (TX) or 80% midjejunoileal resection (RX). Rats were pair fed ± blockade of endogenous GSH synthesis with buthionine sulfoximine (BSO). Indexes of colonic growth, proliferation, and apoptosis and GSH/GSSG and Cys/CySS redox potentials (Eh) were determined. RX significantly increased colonic crypt depth, number of cells per crypt, and epithelial cell proliferation [crypt cell bromodeoxyuridine (BrdU) incorporation]. Administration of BSO markedly decreased colonic mucosal GSH, GSSG, and Cys concentrations in both TX and RX groups, with a resultant oxidation of GSH/GSSG and Cys/CySS Eh. BSO did not alter colonic crypt cell apoptosis but significantly increased all colonic mucosal growth indexes (crypt depth, cells/crypt, and BrdU incorporation) in both TX and RX groups in a time- and dose-dependent manner. BSO significantly decreased plasma GSH and GSSG, oxidized GSH/GSSG Eh, and increased plasma Cys and CySS concentrations. Collectively, these data provide in vivo evidence indicating that oxidized colonic mucosal redox status stimulates colonic mucosal growth in rats. The data also suggest that GSH is required to maintain normal colonic and plasma Cys/CySS homeostasis in these animal models.

scholarly journals Local Glutathione Redox Status Does Not Regulate Ileal Mucosal Growth after Massive Small Bowel Resection in Rats

2007 ◽  
Vol 137 (2) ◽  
pp. 320-325 ◽  
Author(s):  
Junqiang Tian ◽  
Naohiro Washizawa ◽  
Li H. Gu ◽  
Marc S. Levin ◽  
Lihua Wang ◽  
...  
Keyword(s):  
Small Bowel ◽  
Bowel Resection ◽  
Small Bowel Resection ◽  
Redox Status ◽  
Mucosal Growth ◽  
Glutathione Redox ◽  
Massive Small Bowel Resection

Dehydroandrographolide Inhibits Osteosarcoma Cell Growth and Metastasis by Targeting SATB2-mediated EMT

2019 ◽  
Vol 19 (14) ◽  
pp. 1728-1736
Author(s):  
Xuefeng Liu ◽  
Yonggang Fan ◽  
Jing Xie ◽  
Li Zhang ◽  
Lihua Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Wound Healing ◽  
Cell Growth ◽  
Brdu Incorporation ◽  
Migration And Invasion ◽  
Therapeutic Drug ◽  
Osteosarcoma Cell ◽  
Dependent Manner ◽  
Inhibition Of Proliferation ◽  
Predominant Component

Background:The 12-hydroxy-14-dehydroandrographolide (DP) is a predominant component of the traditional herbal medicine Andrographis paniculata (Burm. f.) Nees (Acanthaceae). Recent studies have shown that DP exhibits potent anti-cancer effects against oral and colon cancer cells.Objective:This investigation examined the potential effects of DP against osteosarcoma cell.Methods:A cell analyzer was used to measure cell viability. The cell growth and proliferation were performed by Flow cytometry and BrdU incorporation assay. The cell migration and invasion were determined by wound healing and transwell assay. The expression of EMT related proteins was examined by Western blot analysis.Results:In this study, we found that DP treatment repressed osteosarcoma (OS) cell growth in a dose-dependent manner. DP treatment significantly inhibited OS cell proliferation by arresting the cell cycle at G2/M phase. In addition, DP treatment effectively inhibited the migration and invasion abilities of OS cells through wound healing and Transwell tests. Mechanistic studies revealed that DP treatment effectively rescued the epithelialmesenchymal transition (EMT), while forced expression of SATB2 in OS cells markedly reversed the pharmacological effect of DP on EMT.Conclusion:Our data demonstrated that DP repressed OS cell growth through inhibition of proliferation and cell cycle arrest; DP also inhibited metastatic capability of OS cells through a reversal of EMT by targeting SATB2. These findings demonstrate DP’s potential as a therapeutic drug for OS treatment.

Vitamin A deficiency inhibits intestinal adaptation by modulating apoptosis, proliferation, and enterocyte migration

2003 ◽  
Vol 285 (2) ◽  
pp. G424-G432 ◽  
Author(s):  
Deborah A. Swartz-Basile ◽  
Lihua Wang ◽  
Yuzhu Tang ◽  
Henry A. Pitt ◽  
Deborah C. Rubin ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Small Bowel ◽  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Intestinal Adaptation ◽  
Collagen Iv ◽  
Crypt Cell ◽  
Migration Rates ◽  
Crypt Cell Proliferation ◽  
Extracellular Matrix Components

In a prior study, vitamin A-deficient rats subjected to submassive small bowel resections did not mount a normal intestinal adaptive response by 10 days postoperatively, although adaptive increases in crypt cell proliferation were not attenuated and there were no differences in apoptotic indexes. The present study was designed to address the mechanisms by which vitamin A status effects adaptation by analyzing proliferation, apoptosis, and enterocyte migration in the early postoperative period (16 and 48 h) in vitamin A-sufficient, -deficient, and partially replenished sham-resected and resected rats. At 16 h postresection, apoptosis was significantly greater in the remnant ileum of resected vitamin A-deficient rats compared with the sufficient controls. Crypt cell proliferation was increased by resection in all dietary groups at both timepoints. However, at 48 h postresection, proliferation was significantly decreased in the vitamin A-deficient and partially replenished rats. By 48 h after resection, vitamin A deficiency also reduced enterocyte migration rates by 44%. This occurred in conjunction with decreased immunoreactive collagen IV at 48 h and 10 days postoperation. Laminin expression was also reduced by deficiency at 10 days postresection, whereas fibronectin and pancadherin were unchanged at 48 h and 10 days. These studies indicate that vitamin A deficiency inhibits intestinal adaptation following partial small bowel resection by reducing crypt cell proliferation, by enhancing early crypt cell apoptosis, and by markedly reducing enterocyte migration rates, which may be related to changes in the expression of collagen IV and other extracellular matrix components.

scholarly journals Identification of Wild-Derived Inbred Mouse Strains Highly Susceptible to Monkeypox Virus Infection for Use as Small Animal Models

2010 ◽  
Vol 84 (16) ◽  
pp. 8172-8180 ◽  
Author(s):  
Jeffrey L. Americo ◽  
Bernard Moss ◽  
Patricia L. Earl
Keyword(s):  
Animal Models ◽  
B Lymphocyte ◽  
Inbred Mouse ◽  
Lethal Dose ◽  
Small Animal ◽  
Congo Basin ◽  
Mouse Strains ◽  
Dependent Manner ◽  
Inbred Mouse Strains ◽  
Monkeypox Virus

ABSTRACT Infection with monkeypox virus (MPXV) causes disease manifestations in humans that are similar, although usually less severe, than those of smallpox. Since routine vaccination for smallpox ceased more than 30 years ago, there is concern that MPXV could be used for bioterrorism. Thus, there is a need to develop animal models to study MPXV infection. Accordingly, we screened 38 inbred mouse strains for susceptibility to MPXV. Three highly susceptible wild-derived inbred strains were identified, of which CAST/EiJ was further developed as a model. Using an intranasal route of infection with an isolate of the Congo Basin clade of MPXV, CAST/EiJ mice exhibited weight loss, morbidity, and death in a dose-dependent manner with a calculated 50% lethal dose (LD50) of 680 PFU, whereas there were no deaths of BALB/c mice at a 10,000-fold higher dose. CAST/EiJ mice exhibited greater MPXV sensitivity when infected via the intraperitoneal route, with an LD50 of 14 PFU. Both routes resulted in MPXV replication in the lung, spleen, and liver. Intranasal infection with an isolate of the less-pathogenic West African clade yielded an LD50 of 7,600 PFU. The immune competence of CAST/EiJ mice was established by immunization with vaccinia virus, which induced antigen-specific T- and B-lymphocyte responses and fully protected mice from lethal doses of MPXV. The new mouse model has the following advantages for studying pathogenesis of MPXV, as well as for evaluation of potential vaccines and therapeutics: relative sensitivity to MPXV through multiple routes, genetic homogeneity, available immunological reagents, and commercial production.

Virgin Coconut (Cocos nucifera) Oil Attenuates Rotenone-Induced Toxicity in Fruit Flies (Drosophila melanogaster)

2021 ◽  
Vol 2 (1) ◽  
pp. 26-37
Author(s):  
O.O. Dosumu ◽  
◽  
E.N. Akang ◽  
O.K. Idowu ◽  
G.J. Adeyemi
Keyword(s):  
Drosophila Melanogaster ◽  
Cocos Nucifera ◽  
Coconut Oil ◽  
Redox Status ◽  
Fruit Flies ◽  
Dependent Manner ◽  
Toxicity Assay ◽  
Behavioural Test ◽  
Locomotor Deficits ◽  
Dose Dependent

Background: Parkinson's disease (PD) is a multifactorial neurodegenerative disease with pathogenic mechanisms traceable to oxidative damage and mitochondrial dysfunction. Rotenone, a chemical compound commonly found in pesticides, has been found to inhibit mitochondrial complex-I and initiate PD-like symptoms in mammals and several invertebrates. Virgin Coconut Oil (VCNO) obtained from the coconut fruit has been found to possess anti-oxidative and anti-inflammatory properties. Objectives: The present study evaluated the effect of VCNO on rotenone-induced Parkinsonism in fruit flies- Drosophila melanogaster (D. melanogaster). Methods: Canton special (CS) strains of D. melanogaster, aged between 1 to 3 days were orally exposed for 7 days to 0, 250, 500 and 750 μM rotenone diet for toxicity assay, and 0, 2.5, 5 and 10 % w/w VCNO diet for longevity assay. Thereafter, 5 % VCNO diet was selected for evaluation against 500 μM rotenone. Subsequently, behavioural test (negative geotaxis), markers for redox status and enzyme activities were evaluated. Results: The results showed that rotenone induced toxicity in the flies, while VCNO increased the lifespan of D. melanogaster in a dose-dependent manner. In addition, VCNO ameliorated rotenone-induced locomotor deficits, elevated MDA, as well as the depleted GSH levels. It also mitigated the inhibited activities of SOD, CAT and ATPase in the flies. Conclusions: VCNO protected D. melanogaster against rotenone-induced toxicity by extending longevity, preventing locomotor deficits and reducing oxidative stress.

Vitamin D/VDR signaling inhibits colitis by suppressing HIF-1α activation in colonic epithelial cells

2021 ◽  
Author(s):  
Gang Xue ◽  
Ruifang Gao ◽  
Zhuanzhuan Liu ◽  
Na Xu ◽  
Yong Cao ◽  
...  
Keyword(s):  
Vitamin D ◽  
Animal Models ◽  
Epithelial Cells ◽  
Dextran Sulfate ◽  
Hypoxia Inducible Factor ◽  
Dependent Manner ◽  
Trinitrobenzenesulfonic Acid ◽  
Colonic Epithelial Cells ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Vitamin D/vitamin D receptor (VDR) signaling is reported to have a protective effect on the onset or progression of inflammatory bowel diseases (IBD) and hypoxia-inducible factor 1α (HIF-1α) activation is demonstrated to be closely associated with chemical-induced colitis. However, the association between vitamin D/VDR signaling and HIF-1α on IBD development remains a mystery. Here, we showed that HIF-1α expression was largely increased in the colonic epithelial cells of diseased tissues from ulcerative colitis (UC) patients. Consistently, HIF-1α activation was also improved in colonic epithelial cells upon TNFα treatment in a NF-κB pathway-dependent manner. HIF-1α inhibitors treatments ameliorated 2,4,6-trinitrobenzenesulfonic acid (TNBS)- or dextran sulfate sodium (DSS)-induced colitis in animal models. In cell or colitis animal models, vitamin D/VDR signaling suppressed HIF-1α overexpression in colonic epithelial cells via regulating NF-κB pathway, resulting in the inhibition of IFNγ and IL-1β overproductions in these cells. Collectively, these data suggest that vitamin D/VDR signaling relieves colitis development in animal models, at least in part, by suppressing HIF-1α expression in colonic epithelial cells.

Somatostatin induces ectopic activity fronts via a local intestinal mechanism during fed state or pentagastrin

1986 ◽  
Vol 250 (2) ◽  
pp. G149-G154
Author(s):  
E. Schippers ◽  
J. Janssens ◽  
G. Vantrappen ◽  
M. Vandeweerd ◽  
T. L. Peeters
Keyword(s):  
Small Bowel ◽  
Myoelectric Activity ◽  
Dependent Manner ◽  
Ectopic Activity ◽  
Fed State ◽  
Small Bowel Motility ◽  
Bipolar Electrodes ◽  
Jejunal Segment ◽  
Small Branch ◽  
Local Release

The effect of local intra-arterial infusions of somatostatin on small bowel motility in the postprandial period and during an intravenous pentagastrin infusion was studied in five dogs. A Silastic catheter was implanted in a small branch of the superior mesenteric artery perfusing a 5-to 10-cm jejunal segment located 30-40 cm distally to Treitz. Small bowel myoelectric activity was recorded by means of a series of bipolar electrodes implanted subserosally along the small intestine. Experiments were started 2 wk after surgery and were performed in conscious animals. Intra-arterial infusion of somatostatin induced activity fronts in the fed state and during intravenous pentagastrin infusion in a dose-dependent manner. These activity fronts always started at or just below the perfused segment, migrated distally over the remaining small bowel, and were superimposed on the fed pattern. We conclude that local administration of somatostatin is able to initiate normally migrating ectopic activity fronts, despite the presence of neural and hormonal factors that control the fed state. Local release of somatostatin might be involved in the initiation of spontaneously occurring activity fronts.

scholarly journals Oxidative Stress Implications in the Affective Disorders: Main Biomarkers, Animal Models Relevance, Genetic Perspectives, and Antioxidant Approaches

2016 ◽  
Vol 2016 ◽  
pp. 1-25 ◽  
Author(s):  
Ioana Miruna Balmus ◽  
Alin Ciobica ◽  
Iulia Antioch ◽  
Romeo Dobrin ◽  
Daniel Timofte
Keyword(s):  
Oxidative Stress ◽  
Animal Models ◽  
Affective Disorders ◽  
Dependent Manner ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Oxidative Balance ◽  
Oxidative Stress Status ◽  
Collateral Effect ◽  
Central Nervous System Impairment

The correlation between the affective disorders and the almost ubiquitous pathological oxidative stress can be described in a multifactorial way, as an important mechanism of central nervous system impairment. Whether the obvious changes which occur in oxidative balance of the affective disorders are a part of the constitutive mechanism or a collateral effect yet remains as an interesting question. However it is now clear that oxidative stress is a component of these disorders, being characterized by different aspects in a disease-dependent manner. Still, there are a lot of controversies regarding the relevance of the oxidative stress status in most of the affective disorders and despite the fact that most of the studies are showing that the affective disorders development can be correlated to increased oxidative levels, there are various studies stating that oxidative stress is not linked with the mood changing tendencies. Thus, in this minireview we decided to describe the way in which oxidative stress is involved in the affective disorders development, by focusing on the main oxidative stress markers that could be used mechanistically and therapeutically in these deficiencies, the genetic perspectives, some antioxidant approaches, and the relevance of some animal models studies in this context.

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