Viscoelastic Emulsion Improved the Bioaccessibility and Oral Bioavailability of Crystalline Compound: A Mechanistic Study Using in Vitro and in Vivo Models

2015 ◽  
Vol 12 (7) ◽  
pp. 2229-2236 ◽  
Author(s):  
Yuwen Ting ◽  
Yike Jiang ◽  
Yaqi Lan ◽  
Chunxin Xia ◽  
Zhenyu Lin ◽  
...  
Keyword(s):  
Oral Bioavailability ◽  
Mechanistic Study ◽  
Crystalline Compound ◽  
In Vivo Models ◽  
Compound A

scholarly journals Vanadium pentoxide (V2O5) induced mucin production by airway epithelium

2011 ◽  
Vol 301 (1) ◽  
pp. L31-L39 ◽  
Author(s):  
Dongfang Yu ◽  
Dianne M. Walters ◽  
Lingxiang Zhu ◽  
Pak-Kei Lee ◽  
Yin Chen
Keyword(s):  
Vanadium Pentoxide ◽  
Mapk Pathway ◽  
Mechanistic Study ◽  
Chronic Obstructive ◽  
In Vivo Models ◽  
Mucin Production ◽  
Airway Diseases ◽  
Chronic Airway

Exposure to environmental pollutants has been linked to various airway diseases and disease exacerbations. Almost all chronic airway diseases such as chronic obstructive pulmonary disease and asthma are caused by complicated interactions between gene and environment. One of the major hallmarks of those diseases is airway mucus overproduction (MO). Excessive mucus causes airway obstruction and significantly increases morbidity and mortality. Metals are major components of environmental particulate matters (PM). Among them, vanadium has been suggested to play an important role in PM-induced mucin production. Vanadium pentoxide (V2O5) is the most common commercial source of vanadium, and it has been associated with occupational chronic bronchitis and asthma, both of which are MO diseases. However, the underlying mechanism is not entirely clear. In this study, we used both in vitro and in vivo models to demonstrate the robust inductions of mucin production by V2O5. Furthermore, the follow-up mechanistic study revealed a novel v-raf-1 murine leukemia viral oncogene homolog 1-IKK-NF-κB pathway that mediated V2O5-induced mucin production. Most interestingly, the reactive oxygen species and the classical mucin-inducing epidermal growth factor receptor (EGFR)-MAPK pathway appeared not to be involved in this process. Thus the V2O5-induced mucin production may represent a novel EGFR-MAPK-independent and environmental toxicant-associated MO model. Complete elucidation of the signaling pathway in this model will not only facilitate the development of the treatment for V2O5-associated occupational diseases but also advance our understanding on the EGFR-independent mucin production in other chronic airway diseases.

scholarly journals Assessment of In Vitro Bioaccessibility and In Vivo Oral Bioavailability as Complementary Tools to Better Understand the Effect of Cooking on Methylmercury, Arsenic, and Selenium in Tuna

Toxics ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 27
Author(s):  
Tania Charette ◽  
Danyel Bueno Dalto ◽  
Maikel Rosabal ◽  
J. Jacques Matte ◽  
Marc Amyot
Keyword(s):  
Oral Bioavailability ◽  
Fish Muscle ◽  
In Vitro Models ◽  
In Vivo Studies ◽  
In Vivo Models ◽  
Exposure Pathway ◽  
In Vitro Bioaccessibility ◽  
Kinetics Of

Fish consumption is the main exposure pathway of the neurotoxicant methylmercury (MeHg) in humans. The risk associated with exposure to MeHg may be modified by its interactions with selenium (Se) and arsenic (As). In vitro bioaccessibility studies have demonstrated that cooking the fish muscle decreases MeHg solubility markedly and, as a consequence, its potential absorption by the consumer. However, this phenomenon has yet to be validated by in vivo models. Our study aimed to test whether MeHg bioaccessibility can be used as a surrogate to assess the effect of cooking on MeHg in vivo availability. We fed pigs raw and cooked tuna meals and collected blood samples from catheters in the portal vein and carotid artery at: 0, 30, 60, 90, 120, 180, 240, 300, 360, 420, 480 and 540 min post-meal. In contrast to in vitro models, pig oral bioavailability of MeHg was not affected by cooking, although the MeHg kinetics of absorption was faster for the cooked meal than for the raw meal. We conclude that bioaccessibility should not be readily used as a direct surrogate for in vivo studies and that, in contrast with the in vitro results, the cooking of fish muscle did not decrease the exposure of the consumer to MeHg.

scholarly journals Correction to Assessment of Oral Bioavailability and Biotransformation of Emulsified Nobiletin Using In Vitro and In Vivo Models

2020 ◽  
Vol 68 (44) ◽  
pp. 12503-12503
Author(s):  
Man Zhang ◽  
Konglong Feng ◽  
Guiying Huang ◽  
Yanping Xin ◽  
Jie Xiao ◽  
...  
Keyword(s):  
Oral Bioavailability ◽  
In Vivo Models

scholarly journals Evaluation of a Yeast Hydrolysate from a Novel Strain of Saccharomyces cerevisiae for Mycotoxin Mitigation using In Vitro and In Vivo Models

Toxins ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 7
Author(s):  
Paul Gerard Bruinenberg ◽  
Mathieu Castex
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Plasma Concentration ◽  
Oral Bioavailability ◽  
Oral Absorption ◽  
Disease Risk ◽  
In Vivo Models ◽  
Monogastric Animal ◽  
Yeast Hydrolysate

Mycotoxicoses in animals are caused by exposure to mycotoxin-contaminated feeds. Disease risk is managed using dietary adsorbing agents which reduce oral bioavailability. The objective of this work was to evaluate the efficacy of three selected yeast products as mycotoxin binders using in vitro and in vivo models. Their capacity to adsorb deoxynivalenol (DON), zearalenone (ZEA), and ochratoxin A (OTA) was evaluated using an in vitro model designed to simulate the pH conditions during gastric passage in a monogastric animal. Results showed that only one product, an enzymatic yeast hydrolysate (YHY) of a novel strain Saccharomyces cerevisiae, adsorbed about 45% of DON in solution. Next, we determined the effect of YHY on oral absorption of a DON, ZEA, and OTA mixture using a toxicokinetic model in swine. Toxicokinetic modeling of the plasma concentration-time profiles of DON, OTA, and zearalenone-glucuronide (ZEA-GlcA) showed that YHY tended to reduce the maximal plasma concentration of OTA by 17%. YHY did not reduce oral bioavailability of OTA, DON, and ZEA-GlcA. Within the context of this experiment, and despite some positive indications from both the in vitro and in vivo models employed, we conclude that the YHY prototype was not an effective agent for multiple mycotoxin adsorption.

Assessment of Oral Bioavailability and Biotransformation of Emulsified Nobiletin Using In Vitro and In Vivo Models

2020 ◽  
Vol 68 (41) ◽  
pp. 11412-11420 ◽  
Author(s):  
Man Zhang ◽  
Konglong Feng ◽  
Guiying Huang ◽  
Yanping Xin ◽  
Jie Xiao ◽  
...  
Keyword(s):  
Oral Bioavailability ◽  
In Vivo Models

scholarly journals Isopsoralen ameliorates rheumatoid arthritis by targeting MIF

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Yi Han ◽  
Jinguang Wang ◽  
Shufeng Li ◽  
Yi Li ◽  
Yongli Zhang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Therapeutic Potential ◽  
Mechanistic Study ◽  
Network Pharmacology ◽  
In Vivo Models ◽  
Inflammatory Phenotype ◽  
Anti Inflammatory ◽  
Cellular Thermal Shift Assay

Abstract Background Isopsoralen (IPRN), one of the active ingredients of Psoralea corylifolia Linn, has anti-inflammatory properties. We attempted to investigate the inhibitory effects of IPRN on rheumatoid arthritis (RA) and characterize its potential mechanism. Methods RA fibroblast-like synoviocytes (FLSs) and mice with collagen-induced arthritis (CIA) were used as in vitro and in vivo models to analyze the antiarthritic effect of IPRN. Histological analysis of the inflamed joints from mice with CIA was performed using microcomputed tomography (micro-CT) and hematoxylin-eosin (HE) staining. RNA sequencing (RNA-Seq), network pharmacology analysis, molecular docking, drug affinity responsive target stability (DARTS) assay, and cellular thermal shift assay (CETSA) were performed to evaluate the targets of IPRN. Results IPRN ameliorated the inflammatory phenotype of RA FLSs by inhibiting their cytokine production, migration, invasion, and proangiogenic ability. IPRN also significantly reduced the severity of CIA in mice by decreasing paw thickness, arthritis score, bone damage, and serum inflammatory cytokine levels. A mechanistic study demonstrated that macrophage migration inhibitory factor (MIF), a key protein in the inflammatory process, was the specific target by which IPRN exerted its anti-inflammatory effects in RA FLSs. Conclusion Our study demonstrates the antiarthritic effect of IPRN, which suggests the therapeutic potential of IPRN in RA.

Using in Vitro and in Vivo Models To Evaluate the Oral Bioavailability of Nutraceuticals

2015 ◽  
Vol 63 (5) ◽  
pp. 1332-1338 ◽  
Author(s):  
Yuwen Ting ◽  
Qin Zhao ◽  
Chunxin Xia ◽  
Qingrong Huang
Keyword(s):  
Oral Bioavailability ◽  
In Vivo Models

Kinetics of Various 99mTc-Sn-Pyrophosphate Compounds in the Rat

1977 ◽  
Vol 16 (04) ◽  
pp. 157-162 ◽  
Author(s):  
C. Schümichen ◽  
B. Mackenbrock ◽  
G. Hoffmann
Keyword(s):  
Normal Saline ◽  
Half Life ◽  
Compound A ◽  
Short Half Life ◽  
Low Concentrations ◽  
The Stability ◽  
Kinetics Of ◽  
In Vitro Stability

SummaryThe bone-seeking 99mTc-Sn-pyrophosphate compound (compound A) was diluted both in vitro and in vivo and proved to be unstable both in vitro and in vivo. However, stability was much better in vivo than in vitro and thus the in vitro stability of compound A after dilution in various mediums could be followed up by a consecutive evaluation of the in vivo distribution in the rat. After dilution in neutral normal saline compound A is metastable and after a short half-life it is transformed into the other 99mTc-Sn-pyrophosphate compound A is metastable and after a short half-life in bone but in the kidneys. After dilution in normal saline of low pH and in buffering solutions the stability of compound A is increased. In human plasma compound A is relatively stable but not in plasma water. When compound B is formed in a buffering solution, uptake in the kidneys and excretion in urine is lowered and blood concentration increased.It is assumed that the association of protons to compound A will increase its stability at low concentrations while that to compound B will lead to a strong protein bond in plasma. It is concluded that compound A will not be stable in vivo because of a lack of stability in the extravascular space, and that the protein bond in plasma will be a measure of its in vivo stability.

Melatonin modifies tumor hypoxia and metabolism by inhibiting HIF-1α and energy metabolic pathway in the in vitro and in vivo models of breast cancer

2019 ◽  
Vol 2 (4) ◽  
pp. 83-98 ◽  
Author(s):  
André De Lima Mota ◽  
Bruna Vitorasso Jardim-Perassi ◽  
Tialfi Bergamin De Castro ◽  
Jucimara Colombo ◽  
Nathália Martins Sonehara ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Glucose Metabolism ◽  
Tumor Growth ◽  
Tumor Cells ◽  
Carbonic Anhydrases ◽  
In Vivo Models ◽  
Ca Ix ◽  
Gene And Protein Expression

Breast cancer is the most common cancer among women and has a high mortality rate. Adverse conditions in the tumor microenvironment, such as hypoxia and acidosis, may exert selective pressure on the tumor, selecting subpopulations of tumor cells with advantages for survival in this environment. In this context, therapeutic agents that can modify these conditions, and consequently the intratumoral heterogeneity need to be explored. Melatonin, in addition to its physiological effects, exhibits important anti-tumor actions which may associate with modification of hypoxia and Warburg effect. In this study, we have evaluated the action of melatonin on tumor growth and tumor metabolism by different markers of hypoxia and glucose metabolism (HIF-1α, glucose transporters GLUT1 and GLUT3 and carbonic anhydrases CA-IX and CA-XII) in triple negative breast cancer model. In an in vitro study, gene and protein expressions of these markers were evaluated by quantitative real-time PCR and immunocytochemistry, respectively. The effects of melatonin were also tested in a MDA-MB-231 xenograft animal model. Results showed that melatonin treatment reduced the viability of MDA-MB-231 cells and tumor growth in Balb/c nude mice (p <0.05). The treatment significantly decreased HIF-1α gene and protein expression concomitantly with the expression of GLUT1, GLUT3, CA-IX and CA-XII (p <0.05). These results strongly suggest that melatonin down-regulates HIF-1α expression and regulates glucose metabolism in breast tumor cells, therefore, controlling hypoxia and tumor progression. 

Sign in / Sign up

Export Citation Format

Share Document