Oral in vivo Bactofection in Dextran Sulfate Sodium Treated Female Wistar Rats

Colitis is a multifactorial disorder that mostly occurs in the gastrointestinal tract. Despite improvements in mucosal inflammation research, little is known regarding the small bioactive molecules that are beneficial for regulating T cells and colon cell activity. 6,7,4′-trihydroxyflavanone (THF) is a flavanone that possesses anti-osteoclastogenesis activity and exerts protective effects against methamphetamine-induced immunotoxicity. Whether THF mitigates intestinal inflammation by regulating T cells and colon cell activity remains unknown. In the present study, Jurkat and HT-29 cells were used for in vitro experiments, and dextran sulfate sodium (DSS)-induced colitis model in mice was used for in vivo experiment. We observed that THF did not have a negative effect on the viability of Jurkat and HT-29 cells. Quantitative PCR and Western blot analysis revealed that THF regulates the activity of Jurkat cells and HT-29 cells via the NFκB and MAPK pathways under stimulated conditions. In the DSS-induced colitis model, oral administration of THF attenuated the manifestations of DSS-induced colitis, including a reduction in body weight, shrinkage of the colon, and enhanced expression of pro-inflammatory cytokines in the colon and mesenteric lymph nodes. These data suggest that THF alleviates DSS-induced colitis by modulating the activity of T cells and colon cells in vivo.

Download Full-text

SUPPRESSION EFFECT OF MAHKOTA DEWA (PHALERIA MACROCARPA) LEAF EXTRACT IN CHITOSAN NANOPARTICLES ON THE SMALL INTESTINE OF DEXTRAN SULFATE SODIUM-INDUCED MICE: FOCUS ON MITOSIS AND HYPERPLASIA

Asian Journal of Pharmaceutical and Clinical Research ◽

10.22159/ajpcr.2018.v11i6.24159 ◽

2018 ◽

Vol 11 (6) ◽

pp. 118

Author(s):

Kusmardi Kusmardi ◽

Arif Ramadhan Tamzir ◽

Santi Widiasari ◽

Ari Estuningtyas

Keyword(s):

Small Intestine ◽

Leaf Extract ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Chitosan Nanoparticles ◽

Negative Control ◽

Suppression Effect ◽

Significant Difference ◽

Phaleria Macrocarpa

Objective: The incidence of small intestine cancer (SIC) is rising despite available preventive measures. Kaempferol and quercetin are a potential chemopreventive agent for SIC, but in vivo findings are inconclusive. We aim to study the effects of kaempferol and quercetin on colitis-associated small intestine carcinogenesis in mice.Methods: Suppression effect was tested using mice divided into 6 groups of treatment, i.e.; normal (N) group, negative control (NC), leaf extract (medium dose [MD]) dose 12.5 and 25 mg/kg body weight (BW), leaf extract chitosan and nanoparticle of mahkota dewa (NPMD) dose 6.25 and 12.5 mg/kg BW. Dextran sulfate sodium induction of 1% w/v was administered through drinking water for 6 weeks of treatment. The suppression effect was observed histopathologically by counting the mitotic cells and hyperplasia cells of the crypt of small intestine with hematoxylin-eosin staining.Results: Mitosis cells mean of NC group was not significant difference either with MD 12.5 (p=0.394) or MD 6.5 (p=0.310). However, mitosis cell mean appears to be lower in the NPMD 12.5 (p=0.09) and NPMD 6.25 (p=0.05) groups than the NC group. There was a significant difference among the mean of hyperplasia NC group and MD and also NPMD group. Significant difference also can be showed between MD 12.5 and MD 25 (p=0.026), and between NPMD 6.25 and NPMD 12.5 (p=0.002), and between MD 12.5 and NPMD 12.5 (p=0.002).Conclusion: Our results demonstrate suppression of hyperplasia small intestine by either nanoparticle or extract of Phaleria macrocarpa extracts. The suppression of mitosis was showed by administration of nanoparticle.

Download Full-text

Lactobacillus reuteri Ameliorates Intestinal Inflammation and Modulates Gut Microbiota and Metabolic Disorders in Dextran Sulfate Sodium-Induced Colitis in Mice

Nutrients ◽

10.3390/nu12082298 ◽

2020 ◽

Vol 12 (8) ◽

pp. 2298

Author(s):

Gang Wang ◽

Shuo Huang ◽

Shuang Cai ◽

Haitao Yu ◽

Yuming Wang ◽

...

Keyword(s):

Gut Microbiota ◽

Metabolic Disorders ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Lactobacillus Reuteri ◽

Intestinal Inflammation ◽

Intestinal Bacteria ◽

Ht 29

Lactobacillus reuteri, a commensal intestinal bacteria, has various health benefits including the regulation of immunity and intestinal microbiota. We examined whether L. reuteri I5007 could protect mice against colitis in ameliorating inflammation, modulating microbiota, and metabolic composition. In vitro, HT-29 cells were cultured with L. reuteri I5007 or lipopolysaccharide treatment under three different conditions, i.e., pre-, co- (simultaneous), and posttreatment. Pretreatment with L. reuteri I5007 effectively relieves inflammation in HT-29 cells challenged with lipopolysaccharide. In vivo, mice were given L. reuteri I5007 by gavage throughout the study, starting one week prior to dextran sulfate sodium (DSS) treatment for one week followed by two days without DSS. L. reuteri I5007 improved DSS-induced colitis, which was confirmed by reduced weight loss, colon length shortening, and histopathological damage, restored the mucus layer, as well as reduced pro-inflammatory cytokines levels. Analysis of 16S rDNA sequences and metabolome demonstrates that L. reuteri I5007 significantly alters colonic microbiota and metabolic structural and functional composition. Overall, the results demonstrate that L. reuteri I5007 pretreatment could effectively alleviate intestinal inflammation by regulating immune responses and altering the composition of gut microbiota structure and function, as well as improving metabolic disorders in mice with colitis.

Download Full-text

Genistein Attenuates Vascular Endothelial Impairment in Ovariectomized Hyperhomocysteinemic Rats

Journal of Biomedicine and Biotechnology ◽

10.1155/2012/730462 ◽

2012 ◽

Vol 2012 ◽

pp. 1-10 ◽

Cited By ~ 6

Author(s):

Panpan Zhen ◽

Qian Zhao ◽

Dandan Hou ◽

Teng Liu ◽

Dongqiao Jiang ◽

...

Keyword(s):

Vascular Endothelium ◽

Wistar Rats ◽

Morphological Changes ◽

Vascular Diseases ◽

Bioactive Compound ◽

Ovariectomized Rats ◽

Vascular Endothelial ◽

Female Wistar Rats ◽

Endothelial Impairment

Hyperhomocysteinemia (HHcy) is a well-known independent risk factor for vascular diseases in the general population. This study was to explore the effect of genistein (GST), a natural bioactive compound derived from legumes, on HHcy-induced vascular endothelial impairment in ovariectomized ratsin vivo. Thirty-two adult female Wistar rats were assigned randomly into four groups (n=8): (a) Con: control; (b) Met: 2.5% methionine diet; (c) OVX + Met: ovariectomy + 2.5% methionine diet; (d) OVX + Met + GST: ovariectomy + 2.5% methionine diet + supplementation with genistein. After 12 wk of different treatment, the rats' blood, toracic aortas and liver samples were collected for analysis. Results showed that high-methionine diet induced both elevation of plasma Hcy and endothelial dysfunction, and ovariectomy deteriorated these injuries. Significant improvement of both functional and morphological changes of vascular endothelium was observed in OVX + Met + GST group; meanwhile the plasma Hcy levels decreased remarkably. There were significant elevations of plasma ET-1 and liver MDA levels in ovariectomized HHcy rats, and supplementation with genistein could attenuate these changes. These results implied that genistein could lower the elevated Hcy levels, and prevent the development of endothelial impairment in ovariectomized HHcy rats. This finding may shed a novel light on the anti-atherogenic activities of genistein in HHcy patients.

Download Full-text

Resistant Starch Modulates In Vivo Colonic Butyrate Uptake and Its Oxidation in Rats with Dextran Sulfate Sodium-Induced Colitis

Journal of Nutrition ◽

10.1093/jn/134.3.493 ◽

2004 ◽

Vol 134 (3) ◽

pp. 493-500 ◽

Cited By ~ 24

Author(s):

Noëlle M. Moreau ◽

Martine M. Champ ◽

Stéphane M. Goupry ◽

Bruno J. Le Bizec ◽

Michel Krempf ◽

...

Keyword(s):

Resistant Starch ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium

Download Full-text

Combination of nanosomal form of doxorubicin, interferon alpha, and nitroglycerin in the threatment of 101.8 glioblastoma in Wistar rats

Antibiotics and Chemotherapy ◽

10.37489/0235-2990-2021-66-9-10-17-23 ◽

2022 ◽

Vol 66 (9-10) ◽

pp. 17-23

Author(s):

V. V. Kudelkina ◽

A. S. Khalansky ◽

A. I. Alekseeva ◽

P. L. Gorelikov ◽

A. M. Kosyreva

Keyword(s):

Wistar Rats ◽

Combined Therapy ◽

High Dose ◽

No Donor ◽

Female Wistar Rats ◽

Median Lifespan ◽

C6 Cell Line ◽

Rat C6 Glioma

The search for effective approaches to the treatment of patients with glioblastoma is one of the difficult tasks of neurooncology; standard methods of therapy show limited results. Combined therapy, which includes different antitumor mechanisms, can increase its effectiveness. The combination of PLGA nanoform of doxorubicin (Dox-PLGA), antitumor cytokine — interferon alfa (IFN-α), and nitrogen oxide (NO) donor nitroglycerin (NG) was investigated in this work both in vitro (rat C6 glioma) and in vivo (rat 101.8 glioblastoma). MTT assay in the C6 cell line showed great cytotoxicity and antiproliferative effect of the combination of IFN-α with Dox-PLGA and NG. The lowest tumour cell survival was observed when using a high dose of IFN-α (10 ng/ml) in mono-mode. In the in vivo experiment, 32 female Wistar rats with 101.8 glioblastoma received therapy in the following modes: Dox-PLGA + NG; Dox-PLGA + IFN-α; Dox- PLGA + IFN-α + NG. There was a significant increase in median survival and life expectancy (ILE) in all groups receiving therapy compared to the group that did not undergo treatment. The longest median lifespan (27 days), survival up to 100 days (1 animal), ILE (131%) were observed in animals that received the combination Dox-PLGA + IFN-α+ NG, compared to the group without treatment, in which the median lifespan was 15 days. Thus, the therapy of experimental glioblastoma both in vivo and in vitro with the combination of Dox-PLGA + IFN-α + NG has the most pronounced therapeutic and antitumor effect, which must be taken into account when developing new more effective methods of treating human glioblastomas.

Download Full-text

Effect of Reoxygenation on the Electrical Stability of the Rat Heart In Vivo: A Chronobiological Study

Physiological Research ◽

10.33549/physiolres.932579 ◽

2013 ◽

pp. S143-S149

Author(s):

P. ŠVORC ◽

A. MAROSSY ◽

P. ŠVORC ◽

M. BUŽGA

Keyword(s):

Body Weight ◽

Tidal Volume ◽

Rat Heart ◽

Ventricular Arrhythmias ◽

Wistar Rats ◽

Pulmonary Ventilation ◽

Electrical Stability ◽

Female Wistar Rats ◽

Light:Dark Cycle

Reoxygenation following hypoxic episodes can increase the risk for the development of ventricular arrhythmias, which, in addition to circadian aspects of reoxygenation arrhythmias has not been studied extensively. The aim of the present study was to evaluate circadian changes in the electrical stability of the rat heart during reoxygenation following a hypoventilatory episode. The electrical stability of the heart, defined in the present study as the ventricular arrhythmia threshold (VAT), was measured at 3 h intervals at clock times 09:00, 12:00, 15:00, 18:00, 21:00, 24:00, 03:00, 06:00 and 09:00 during 20 min hypoventilation (20 breaths/min, tidal volume = 0.5 ml/100 g body weight [n=17]) and subsequent 20 min reoxygenation (50 breaths/min, tidal volume = 1 ml/100 g body weight [n=4]) intervals. The experiments were performed using pentobarbital-anesthetized (40 mg/kg intraperitoneally) female Wistar rats that first underwent a four-week adaptation to a 12 h light:12 h dark regimen. Detailed analysis showed that circadian VATs changed to biphasic rhythms at 10 min of hypoventilation. The VAT circadian rhythms were observed immediately following the commencement of reoxygenation, with the highest values measured between 12:00 and 15:00, and the lowest values between 24:00 and 03:00. These results suggest that myocardial vulnerability is dependent on the light:dark cycle and characteristics of pulmonary ventilation.

Download Full-text

Cinacalcet Targets the Neurokinin-1 Receptor and Inhibits PKCδ/ERK/P65 Signaling to Alleviate Dextran Sulfate Sodium-Induced Colitis

Frontiers in Pharmacology ◽

10.3389/fphar.2021.735194 ◽

2021 ◽

Vol 12 ◽

Author(s):

Yuehong Chen ◽

Huan Liu ◽

Qiuping Zhang ◽

Yubin Luo ◽

Liang Wu ◽

...

Keyword(s):

Signaling Pathway ◽

Inflammatory Cytokines ◽

Structural Integrity ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Therapeutic Effects ◽

Neurokinin 1 Receptor ◽

Neurokinin 1

Objective: Inflammatory bowel disease is an immune-mediated chronic inflammatory disease of the gastrointestinal tract for which curative drugs are currently not available. This study was performed to assess the therapeutic effects of cinacalcet on dextran sulfate sodium (DSS)-induced colitis.Methods: Primary macrophages obtained from bone marrow and the macrophage cell line RAW264.7 were used to examine the inhibitory effect of cinacalcet on cytokine production, the PKCδ/ERK/P65 signaling pathway, and NF-κB P65 translocation. Colitis was induced using DSS to assess the treatment effect of cinacalcet. Bioinformatics approaches were adopted to predict potential targets of cinacalcet, and a drug affinity responsive target stability (DARTs) assay was performed to confirm binding between cinacalcet and potential target.Results:In vivo analysis showed that cinacalcet reduced the disease activity score, prevented shortening of the colon, diminished inflammatory cell infiltration, and protected the structural integrity of the intestinal wall. Cinacalcet also reduced production of the inflammatory cytokines TNFα, IL-1β, and IL-6 in the colon and sera of mice with DSS-induced colitis. In vitro studies revealed that cinacalcet suppressed the translocation of P65 and inhibited production of the inflammatory cytokines IL-1β and IL-6. Mechanistic studies revealed that the target of cinacalcet was neurokinin-1 receptor (NK1R) and their binding was confirmed by a DARTs assay. Furthermore, the inhibition of NK-κB P65 activation was found to occur via the suppression of PKCδ/ERK/P65 signaling mediated by cinacalcet.Conclusion: Cinacalcet inhibits the activation of NF-κB and reduces the production of inflammatory cytokines by suppressing the PKCδ/ERK/P65 signaling pathway via targeting NK1R, suggesting that it can be used to treat inflammatory diseases, particularly colitis.

Download Full-text

Expression, localization, and regulation of aquaporin-1 to -3 in rat urothelia

AJP Renal Physiology ◽

10.1152/ajprenal.00136.2001 ◽

2002 ◽

Vol 282 (6) ◽

pp. F1034-F1042 ◽

Cited By ~ 62

Author(s):

David A. Spector ◽

James B. Wade ◽

Russell Dillow ◽

Deborah A. Steplock ◽

Edward J. Weinman

Keyword(s):

Epithelial Cell ◽

Wistar Rats ◽

Apical Membrane ◽

Water Movement ◽

Bulk Water ◽

In Vivo Studies ◽

Cell Cytoplasm ◽

Aquaporin 1 ◽

Female Wistar Rats

Although mammalian urothelia are generally considered impermeable to constituents of urine, in vivo studies in several species indicate urothelial transport of water and solutes under certain conditions. This study investigates the expression, localization, and regulation of aquaporin (AQP)-1, -2, and -3 in ureteral and bladder tissues in 48-h dehydrated and water-loaded female Wistar rats. Immunoblots of homogenates of whole ureter and bladder identified characteristic ∼28- and 35- to 44-kDa bands for AQP-1, -2, and -3. AQP-1 was localized to capillary and arteriole endothelial cells, whereas AQP-2 and -3 circumferentially lined the epithelial cell membranes except for the apical membrane of the epithelial cells adjacent to the lumens of both ureter and bladder. AQP-2 was also present in epithelial cell cytoplasm. Dehydration resulted in 160–200% increases of AQP-3 signal and 24–49% increases of AQP-2 signal but no change in AQP-1 signal on immunoblots of homogenates of ureters and bladders. AQPs in genitourinary tract urothelia likely play a role in the regulation of epithelial cell volume and osmolality and may play a role in bulk water movement across urothelia.

Download Full-text