scholarly journals POPULATION DYNAMICS OF INTESTINAL EPITHELIA IN THE RAT TWO MONTHS AFTER PARTIAL RESECTION OF THE ILEUM

1963 ◽  
Vol 19 (2) ◽  
pp. 285-291 ◽  
Author(s):  
M. R. Loran ◽  
T. T. Crocker
Keyword(s):  
Tritiated Thymidine ◽  
Partial Resection ◽  
Intestinal Epithelial ◽  
Sprague Dawley ◽  
Intestinal Crypt ◽  
Intestinal Epithelia ◽  
Sprague Dawley Rats ◽  
Feulgen Technique ◽  
Crypt Cells ◽  
Epithelial Growth

Sprague-Dawley rats that had been subjected 2 months previously to partial resection (10 per cent) of the small intestine and an equal number of control rats were injected with tritiated thymidine and sacrificed at intervals during the subsequent 16 hours. Segments of duodenum, jejunum and ileum were prestained by the Feulgen technique and radioautographed. The proportion of crypt cells bearing labeled nuclei, the percentage of labeled crypt cells in mitosis and the appearance of labeled crypt cells on the villi were determined. Comparison of control and resected rats showed that (a) the proportion of intestinal crypt cells incorporating thymidine was considerably greater and uniformly high throughout the shortened intestine, (b) the life cycle of crypt cells was slightly reduced, and was uniform throughout the shortened intestine, and (c) the time during which cells were retained in crypts was markedly reduced. On the basis of persistent, generalized increase in the production of crypt cells, and on prior evidence that the epithelial cells of shortened intestine continue to have a brief life span and evidence of metabolic immaturity, the existence of a humoral factor, tentatively called "intestinal epithelial growth hormone," is postulated.

scholarly journals Cellular Proliferation of Intestinal Epithelia in the Rat Two Months after Partial Resection of the Ileum

1960 ◽  
Vol 7 (4) ◽  
pp. 667-671 ◽  
Author(s):  
M. R. Loran ◽  
T. L. Althausen
Keyword(s):  
Small Intestine ◽  
Cellular Proliferation ◽  
Tritiated Thymidine ◽  
Partial Resection ◽  
Normal Rate ◽  
Cell Renewal ◽  
Sprague Dawley ◽  
Intestinal Epithelia ◽  
Sprague Dawley Rats ◽  
Normal Intestine

Sprague-Dawley rats subjected 2 months previously to partial resection (10 per cent) of the small intestine and their controls were injected with tritiated thymidine and sacrificed at 2 and 23 hours. Segments of the duodenum, jejunum, and ileum were autoradiographed, and the migration of the labelled cells during the period between 2 and 23 hours was measured with an eyepiece micrometer. The cells had migrated 35, 42, and 34 per cent of the total distance from the crypts to the tips of the villi in the control segments of duodenum, ileum, and jejunum respectively, and 43, 90, and 82 per cent, respectively, in similar segments from resected animals. The rate of migration in the portion of the intestine remaining after resection was approximately three times the normal rate in the ileum, twice the normal rate in the jejunum, and showed an increase of one-third in the duodenum. These results demonstrate that the rate of cell renewal is considerably greater in the remaining portion of the intestine of resected animals than in normal intestine. The increased rate of migration after resection, together with the increase in the height of the villi, resulted in an increase in the rate of cell renewal amounting to 141 per cent in the ileum, 114 per cent in the jejunum, and 23 per cent in the duodenum when compared with control segments.

Modified hemoglobins produce venular interendothelial gaps and albumin leakage in the rat mesentery

1999 ◽  
Vol 277 (2) ◽  
pp. H650-H659 ◽  
Author(s):  
Ann L. Baldwin
Keyword(s):  
Actin Cytoskeleton ◽  
Blood Substitutes ◽  
Cell Junctions ◽  
Intestinal Epithelial ◽  
Sprague Dawley ◽  
Filamentous Actin ◽  
Rat Mesentery ◽  
Sprague Dawley Rats ◽  
Albumin Leakage ◽  
Endothelial Gaps

Cross-linked hemoglobin (αα-Hb) and polyethylene glycol (PEG)-conjugated Hb have both been considered as possible “blood substitutes.” Previously, we showed that PEG-Hb extravasates rapidly in the intestinal mucosa and causes transient epithelial sloughing, resulting in temporary opening of the intestinal epithelial barrier. In the present study, the rat mesenteric preparation was used to quantify the effects of the two Hbs on microvascular leakage to albumin and to investigate possible changes in the integrity of the interendothelial cell junctions and the endothelial actin cytoskeleton. In anesthetized Sprague-Dawley rats, the microvasculature of a mesenteric window was perfused with HEPES-buffered saline (HBS) containing 0.5 mg/ml BSA and 2 mg/ml αα-Hb ( n = 16) or PEG-Hb ( n = 5) for 2 or 10 min. Controls ( n = 4) just received HBS-BSA. In some experiments ( n = 9 for αα-Hb ; n = 5 for PEG-Hb), the perfusate was then replaced by FITC-albumin in HBS-BSA for the next 3 min. The vasculature was then perfusion fixed, stained for filamentous actin and for mast cells, and viewed microscopically. In the remaining experiments, the mesenteric microvasculature was stained with silver nitrate to determine the number of endothelial junctional gaps per length of venules. Both Hbs increased the number and area of leaks per micrometer of venular length compared with control, but αα-Hb increased to a greater extent than PEG-Hb. Formation of leaks was accompanied by changes in the endothelial actin cytoskeleton and by an increased number of endothelial gaps. Mast cell degranulation was significantly greater ( P < 0.05) in Hb-treated preparations compared with controls, but there was no direct correlation between sites of degranulation and albumin leakage. These Hbs appear to induce venular leakage in the mesentery by mechanisms similar to those previously observed after treatment with histamine or nitric oxide synthase inhibitors.

scholarly journals Effects of Curcumin on Bioavailability of Dioxin-Like Pollutants in Rats

2021 ◽  
Author(s):  
Delei Cai ◽  
Qing Chen ◽  
Jianlong Han ◽  
Yanhua Song ◽  
Zhen Meng ◽  
...  
Keyword(s):  
Chemical Structure ◽  
Intestinal Epithelial Cells ◽  
Female Rats ◽  
Male Rats ◽  
Intestinal Epithelial ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Similar Chemical ◽  
Small Intestinal ◽  
Detoxification Mechanisms

Abstract In this study, we used Sprague–Dawley rats to observe the intervention effects of curcumin on bioavailability of polychlorinated dibenzo-p-dioxins/furans (PCDD/Fs) and dioxin-like polychlorinated biphenyls (DL-PCBs). We reported the bioavailability of tetra- to hexa-chlorinated PCDD/Fs rose gradually, while that of hepta- and octa-chlorinated PCDD/Fs declined, and no obvious change was found in the bioavailability of DL-PCBs. Curcumin markedly reduced the toxic equivalent (TEQ) of PCDD/Fs in rats, illustrating it might competitively inhibit absorption of PCDD/Fs in small intestinal epithelial cells due to the similar chemical structure (diphenyl) between curcumin and PCDD/Fs. Moreover, curcumin was capable of lowering the TEQ of DL-PCBs in the liver of male rats, but caused no changes in female rats. In conclusion, the prominent decline in the bioavailability of PCDD/Fs and DL-PCBs induced by curcumin may serve as one of the detoxification mechanisms of curcumin for these pollutants.

Microflora-derived polyamines modulate obstruction-induced colonic mucosal hypertrophy

1989 ◽  
Vol 256 (6) ◽  
pp. G1049-G1057 ◽  
Author(s):  
D. L. Osborne ◽  
E. R. Seidel
Keyword(s):  
Colonic Obstruction ◽  
Arginine Decarboxylase ◽  
Local Effect ◽  
Decarboxylase Activity ◽  
Intestinal Epithelial ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Mucosal Response ◽  
Mucosal Hypertrophy

Experiments were designed to determine the role of microflora-derived intraluminal polyamines in the colonic mucosal response to obstruction. Sprague-Dawley rats were treated per os with 0.9% NaCl or a combination of nonabsorbable antibiotics prior to the placement of either a sham or complete colonic obstruction. Sixty-six hours after surgery, wet tissue weight, DNA, RNA, and protein content were all increased in the mucosa proximal to the obstruction in NaCl-treated animals; however, DNA content was the only parameter increased after antibiotics. This induction was a purely local effect as neither hyperplasia nor hypertrophy was observed in the ileum or colon distal to the obstruction. In the NaCl-treated animals, mucosal ornithine decarboxylase activity was not induced until 48 h postsurgery, yet mucosal spermidine concentrations were significantly higher as early as 24 h. Intraluminal bacterial lysine, ornithine, and arginine decarboxylase activities were induced by obstruction but were reduced by antibiotic treatment. [14C]putrescine uptake by intestinal epithelial cells (IEC-6) in culture was blocked by the antibiotics employed in this study, but [14C]-lysine transport was relatively unaffected. These data demonstrate that intraluminal polyamines modulate the trophic response of the colonic mucosa after colonic obstruction.

Comparison of effects of two hemoglobin-based O2carriers on intestinal integrity and microvascular leakage

2002 ◽  
Vol 283 (4) ◽  
pp. H1292-H1301 ◽  
Author(s):  
Ann L. Baldwin ◽  
Elizabeth B. Wiley ◽  
Abdu I. Alayash
Keyword(s):  
Clinical Trials ◽  
The United States ◽  
Blood Substitutes ◽  
Intestinal Epithelial ◽  
Human Hemoglobin ◽  
Sprague Dawley ◽  
Intestinal Integrity ◽  
Sprague Dawley Rats ◽  
The Mean ◽  
Epithelial Disruption

Two “blood substitutes,” a diaspirin cross-linked human hemoglobin [bis(3,5 dibromosalicyl)fumarate, DBBF-Hb] and a bovine polymerized hemoglobin (PolyHbBv), advanced to clinical trials, are used in this study. Previously, we have shown that injection of DBBF-Hb into the rat circulation produces venular leakage and intestinal epithelial disruption. The purpose of this study was to determine whether PolyHbBv, currently approved for veterinary use in the United States, shows similar effects. In anesthetized Sprague-Dawley rats, the mesenteric microvasculature was perfused with DBBF-Hb ( n = 6), PolyHbBv ( n = 5), cyanomet Hb (CNmet-DBBF-Hb), or HEPES-buffered saline with 0.5% bovine serum albumin (HBS-BSA) (controls, n = 7) for 10 min, followed by FITC-albumin for 3 min, and then fixed for microscopy. For DBBF-Hb, the mean leak number per micrometer venule length [2.41 ± 0.33 (±SE) × 10−3] was significantly greater than for PolyHbBv (0.53 ± 0.14 × 10−3), CNmet-DBBF-Hb (0.36 ± 0.14 × 10−3), and HBS-BSA (0.12 ± 0.08 × 10−3) ( P < 0.01). Corresponding quantities for leak area were 0.10 ± 0.03, 0.010 ± 0.003, 0.005 ± 0.003, and 0.02 ± 0.02 μm2/μm. In rats injected with DBBF-Hb ( n = 8), intestinal epithelial integrity was significantly compromised compared with those injected with PolyHbBv ( n = 5) or saline ( n = 6). These results indicate that intravascular PolyHbBv produces significantly less disruption of the intestinal exchange barrier than does DBBF-Hb, probably because the heme is not so easily oxidized.

scholarly journals Molecular Mechanism of Stimulation of Na-K-ATPase by Leukotriene D4 in Intestinal Epithelial Cells

2021 ◽  
Vol 22 (14) ◽  
pp. 7569
Author(s):  
Niraj Nepal ◽  
Subha Arthur ◽  
Molly R. Butts ◽  
Soudamani Singh ◽  
Balasubramanian Palaniappan ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Atpase Activity ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Leukotriene D4 ◽  
Intestinal Crypt ◽  
Calphostin C ◽  
Chronic Intestinal Inflammation ◽  
Crypt Cells ◽  
Stimulation Of

Na-K-ATPase provides a favorable transcellular Na gradient required for the functioning of Na-dependent nutrient transporters in intestinal epithelial cells. The primary metabolite for enterocytes is glutamine, which is absorbed via Na-glutamine co-transporter (SN2; SLC38A5) in intestinal crypt cells. SN2 activity is stimulated during chronic intestinal inflammation, at least in part, secondarily to the stimulation of Na-K-ATPase activity. Leukotriene D4 (LTD4) is known to be elevated in the mucosa during chronic enteritis, but the way in which it may regulate Na-K-ATPase is not known. In an in vitro model of rat intestinal epithelial cells (IEC-18), Na-K-ATPase activity was significantly stimulated by LTD4. As LTD4 mediates its action via Ca-dependent protein kinase C (PKC), Ca levels were measured and were found to be increased. Phorbol 12-myristate 13-acetate (PMA), an activator of PKC, also mediated stimulation of Na-K-ATPase like LTD4, while BAPTA-AM (Ca chelator) and calphostin-C (Cal-C; PKC inhibitor) prevented the stimulation of Na-K-ATPase activity. LTD4 caused a significant increase in mRNA and plasma membrane protein expression of Na-K-ATPase α1 and β1 subunits, which was prevented by calphostin-C. These data demonstrate that LTD4 stimulates Na-K-ATPase in intestinal crypt cells secondarily to the transcriptional increase of Na-K-ATPase α1 and β1 subunits, mediated via the Ca-activated PKC pathway.

Mitochondrial Changes in the Adrenal Glands Following the Administration of 7,12-Dimethylbenzanthracene

1971 ◽  
Vol 29 ◽  
pp. 578-579
Author(s):  
T. M. Murad ◽  
J. R. Leibach ◽  
E. von Haam
Keyword(s):  
Adrenal Glands ◽  
Tritiated Thymidine ◽  
Light And Electron Microscopy ◽  
Breast Tumors ◽  
Sprague Dawley ◽  
Cortical Necrosis ◽  
Intravenous Injections ◽  
Sprague Dawley Rats ◽  
Sudan Iii ◽  
Pre Treatment

Adrenal cortical necrosis and apoplexy have been described by Huggins and Morii to follow single or multiple intravenous injections of 7,12-dimethyl-benzanthracene into female Sprague-Dawley rats. This phenomenon is species- and strain-specific and occurs within a few days after DMBA administration. The mechanism by which the chemical exerts its damaging effect on the adrenals is not known although it has been suggested that the 7-hydroxymethyl derivative produced in the liver is the responsible agent. The adrenal cortical necrosis is dose-related and can be prevented by pre-treatment of the animals with 3-methylcholanthrene or Sudan III.In the present study the adrenal glands from 31 animals which had developed breast tumors after treatment with 7,12-DMBA were studied by light and electron microscopy. Five animals were injected with DMBA and five weeks later were injected with tritiated thymidine three hours before sacrifice. The adrenals from these animals were studied by autoradiography.

scholarly journals Si Shen Wan Regulates Phospholipase Cγ-1 and PI3K/Akt Signal in Colonic Mucosa from Rats with Colitis

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Duan-yong Liu ◽  
Rong Xu ◽  
Min-fang Huang ◽  
Hong-yan Huang ◽  
Xin Wang ◽  
...  
Keyword(s):  
Sulfonic Acid ◽  
Colonic Mucosa ◽  
Intestinal Epithelial Cells ◽  
Experimental Colitis ◽  
Mucosal Injury ◽  
Signal Pathway ◽  
Trinitrobenzene Sulfonic Acid ◽  
Intestinal Epithelial ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

The present study explored the feasible pathway of Si Shen Wan (SSW) in inhibiting apoptosis of intestinal epithelial cells (IECs) by observing activation of phospholipase Cγ-1 (PLC-γ1) and PI3K/Akt signal in colonic mucosa from rats with colitis. Experimental colitis was induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS) in the Sprague-Dawley rats. After SSW was administrated for 7 days after TNBS infusion, western blot showed an increment in levels of PI3K, p-Akt, and IL-23 and a decrement in levels of PLC-γ1 and HSP70 in colonic mucosal injury induced by TNBS. Meanwhile, assessments by ELISA revealed an increment in concentrations of IL-2, IL-6, and IL-17 and a reduction in level of TGF-βafter TNBS challenge. Impressively, treatment with SSW for 7 days significantly attenuated the expressions of PI3K and p-Akt and the secretion of IL-2, IL-6, IL-17, and IL-23 and promoted the activation of PLC-γ1, HSP70, and TGF-β. Our previous studies had demonstrated that SSW restored colonic mucosal ulcers by inhibiting apoptosis of IECs. The present study demonstrated that the effect of SSW on inhibiting apoptosis of IECs was realized probably by activation of PLC-γ1 and suppression of PI3K/Akt signal pathway.

Differentiated intestinal epithelial cells exhibit increased migration through polyamines and myosin II

1999 ◽  
Vol 277 (6) ◽  
pp. G1149-G1158 ◽  
Author(s):  
Jaladanki N. Rao ◽  
Ji Li ◽  
Li Li ◽  
Barbara L. Bass ◽  
Jian-Ying Wang
Keyword(s):  
Cell Migration ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Myosin Ii ◽  
Specific Inhibitor ◽  
Intestinal Epithelial ◽  
Nonmuscle Myosin ◽  
Intestinal Crypt ◽  
Nonmuscle Myosin Ii ◽  
Crypt Cells

Early mucosal restitution is a rapid process by which differentiated intestinal epithelial cells migrate to reseal superficial wounds. However, most of the in vitro studies for restitution employ undifferentiated intestinal crypt cells as a model. The transcription factor, Cdx2, plays an important role in the regulation of intestinal epithelial differentiation. Forced expression of the Cdx2 gene in undifferentiated intestinal crypt cells induces the development of a differentiated phenotype. The current study was designed to determine changes in differentiated intestinal epithelial cell migration after wounding in the stable Cdx2-transfected IEC-6 cells and then to examine involvement of polyamines and nonmuscle myosin II in the process of cell motility. Cdx2-transfected IEC-6 cells were associated with a highly differentiated phenotype and exhibited increased cell migration after wounding. Migration of Cdx2-transfected IEC-6 cells were approximately four times that of nontransfected IEC-6 cells. Migration after wounding was associated with significant increases in polyamine synthesis. Depletion of cellular polyamines by 5 mM α-difluoromethylornithine (DFMO), a specific inhibitor of polyamine biosynthesis, inhibited cell migration without affecting the differentiated phenotype. DFMO also decreased levels of nonmuscle myosin II mRNA and protein and resulted in reorganization of myosin II, along with a marked reduction in stress fibers. Exogenous spermidine given together with DFMO not only returned nonmuscle myosin II levels and cellular distribution toward normal but also restored cell migration to control levels. These results indicate that 1) Cdx2-transfected IEC-6 cells exhibit increased cell migration after wounding and 2) cellular polyamines are absolutely required for stimulation of cell migration in association with their ability to modulate the structural organization of nonmuscle myosin II.

Sign in / Sign up

Export Citation Format

Share Document