scholarly journals Biocompatibility and Degradation Behavior of Molybdenum in an In Vivo Rat Model

Materials ◽  
2021 ◽  
Vol 14 (24) ◽  
pp. 7776
Author(s):  
Antje Schauer ◽  
Christian Redlich ◽  
Jakob Scheibler ◽  
Georg Poehle ◽  
Peggy Barthel ◽  
...  
Keyword(s):  
Vessel Wall ◽  
Degradation Rate ◽  
Degradation Behavior ◽  
C Reactive Protein ◽  
In Vitro Degradation ◽  
Reactive Protein ◽  
Degradation Rates ◽  
In Vivo Degradation

The biocompatibility and degradation behavior of pure molybdenum (Mo) as a bioresorbable metallic material (BMM) for implant applications were investigated. In vitro degradation of a commercially available Mo wire (ø250 µm) was examined after immersion in modified Kokubo’s SBF for 28 days at 37 °C and pH 7.4. For assessment of in vivo degradation, the Mo wire was implanted into the abdominal aorta of female Wistar rats for 3, 6 and 12 months. Microstructure and corrosion behavior were analyzed by means of SEM/EDX analysis. After explantation, Mo levels in serum, urine, aortic vessel wall and organs were investigated via ICP-OES analysis. Furthermore, histological analyses of the liver, kidneys, spleen, brain and lungs were performed, as well as blood count and differentiation by FACS analysis. Levels of the C-reactive protein were measured in blood plasma of all the animals. In vitro and in vivo degradation behavior was very similar, with formation of uniform, non-passivating and dissolving product layers without occurrence of a localized corrosion attack. The in vitro degradation rate was 101.6 µg/(cm2·d) which corresponds to 33.6 µm/y after 28 days. The in vivo degradation rates of 12, 33 and 36 µg/(cm2·d) were observed after 3, 6 and 12 months for the samples properly implanted in the aortic vessel wall. This corresponds with a degradation rate of 13.5 µm/y for the 12-month cohort. However, the magnitude of degradation strongly depended on the implant site, with the wires incorporated into the vessel wall showing the most severe degradation. Degradation of the implanted Mo wire neither induced an increase in serum or urine Mo levels nor were elevated Mo levels found in the liver and kidneys compared with the respective controls. Only in the direct vicinity of the implant in the aortic vessel wall, a significant amount of Mo was found, which, however, was far below the amounts to be expected from degrading wires. No abnormalities were detected for all timepoints in histological and blood analyses compared to the control group. The C-reactive protein levels were similar between all the groups, indicating no inflammation processes. These findings suggest that dissolved Mo from a degrading implant is physiologically transported and excreted. Furthermore, radiographic and µCT analyses revealed excellent radiopacity of Mo in tissues. These findings and the unique combination with its extraordinary mechanical properties make Mo an interesting alternative for established BMMs.

In Vitro and In Vivo Degradation, Mechanical Properties, and Histocompatibility of Weft-Knitted Silk Mesh-Like Grafts

2022 ◽  
Vol 12 (2) ◽  
pp. 411-416
Author(s):  
Liang Tang ◽  
Si-Yu Zhao ◽  
Ya-Dong Yang ◽  
Geng Yang ◽  
Wen-Yuan Zhang ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Simulated Body Fluid ◽  
Body Fluid ◽  
Degradation Rate ◽  
Maximum Load ◽  
Artificial Ligament ◽  
In Vivo Degradation

To investigate the degradation, mechanical properties, and histocompatibility of weft-knitted silk mesh-like grafts, we carried out the In Vitro and In Vivo silk grafts degradation assay. The In Vitro degradation experiment was performed by immersing the silk grafts in simulated body fluid for 1 year, and the results showed that the degradation rate of the silk mesh-like grafts was very slow, and there were few changes in the mechanical properties and quality of the silk mesh-like graft. In Vivo degradation assay was taken by implantation of the silk mesh-like grafts into the subcutaneous muscles of rabbits. At 3, 6, and 12 months postoperation, the rate of mass loss was 19.36%, 31.84%, and 58.77%, respectively, and the maximum load was 63.85%, 34.63%, and 10.76%, respectively of that prior to degradation. The results showed that the degradation rate of the silk graft and the loss of mechanical properties In Vivo were faster than the results obtained in the In Vitro experiments. In addition, there were no significant differences in secretion of serum IL-6 and TNF-α between the experimental and normal rabbits (P >0.05), suggesting no obvious inflammatory reaction. The findings suggest that the weft-knitted silk mesh-like grafts have good mechanical properties, histocompatibility, and In Vivo degradation rate, and therefore represent a candidate material for artificial ligament

scholarly journals Influence of apolipoprotein E genotype and dietary α-tocopherol on redox status and C-reactive protein levels in apolipoprotein E3 and E4 targeted replacement mice

2008 ◽  
Vol 100 (1) ◽  
pp. 44-53 ◽  
Author(s):  
Laia Jofre-Monseny ◽  
Patricia Huebbe ◽  
Inken Stange ◽  
Christine Boesch-Saadatmandi ◽  
Jan Frank ◽  
...  
Keyword(s):  
Apoe Genotype ◽  
Positive Association ◽  
Thiobarbituric Acid ◽  
Redox Status ◽  
C Reactive Protein ◽  
Cvd Risk ◽  
Reactive Protein ◽  
Antioxidant Defence System

The molecular basis of the positive association between apoE4 genotype and CVD remains unclear. There is direct in vitro evidence indicating that apoE4 is a poorer antioxidant relative to the apoE3 isoform, with some indirect in vivo evidence also available. Therefore it was hypothesised that apoE4 carriers may benefit from α-tocopherol (α-Toc) supplementation. Targeted replacement mice expressing the human apoE3 and apoE4 were fed with a diet poor (0 mg/kg diet) or rich (200 mg/kg diet) in α-Toc for 12 weeks. Neither apoE genotype nor dietary α-Toc exerted any effects on the antioxidant defence system, including glutathione, catalase, superoxide dismutase, glutathione peroxidase and glutathione reductase activities. In addition, no differences were observed in mitogen-induced lymphocyte proliferation. α-Toc concentrations were modestly higher in plasma and lower in tissues of apoE4 compared with apoE3 mice, with the greatest differences evident in the lung, suggesting that an apoE4 genotype may reduce α-Toc delivery to tissues. A tendency towards increased plasma F2-isoprostanes in apoE4 mice was observed, while liver thiobarbituric acid-reactive substances did not differ between apoE3 and apoE4 mice. In addition, C-reactive protein (CRP) concentrations were reduced in apoE4 mice indicating that this positive effect on CRP may in part negate the increased CVD risk associated with an apoE4 genotype.

The in vivo and in vitro degradation behavior of poly(trimethylene carbonate)

Biomaterials ◽  
2006 ◽  
Vol 27 (9) ◽  
pp. 1741-1748 ◽  
Author(s):  
Zheng Zhang ◽  
Roel Kuijer ◽  
Sjoerd K. Bulstra ◽  
Dirk W. Grijpma ◽  
Jan Feijen
Keyword(s):  
Degradation Behavior ◽  
Trimethylene Carbonate ◽  
In Vitro Degradation

Degradation of Poly(Anhydride-Co-Imides): Novel Polymers for Orthopedic Applications

1995 ◽  
Vol 394 ◽  
Author(s):  
Kathryn E. Uhrich ◽  
Sobrasua E. M. Ibim ◽  
Cato T. Laurencin ◽  
Robert Langer
Keyword(s):  
Bone Growth ◽  
Subcutaneous Tissue ◽  
Polymer Degradation ◽  
Polymer Backbone ◽  
In Vitro Degradation ◽  
Time Period ◽  
Orthopedic Applications ◽  
In Vivo Degradation

AbstractNovel polymers with good mechanical properties are being developed as degradable matrices for bone growth and regeneration. The poly(anhydride-co-imides) were synthesized from trimellitylimidoglycine and 1,6-bis(p-carboxyphenoxy)hexane in molar compositions of 10:90, 30:70 and 50:50. These polymers have compressive strengths (23–57 MPa), which are similar to human cortical bone. 1 In vitro degradation was performed under acidic (pH 5), physiological (pH 7.4), and basic (pH 10) conditions. The degradation rate increased under basic conditions and by increasing the amount of trimellitylimidoglycine in the polymer backbone. Two erosion zones were observed in the polymers by microscopy. In vivo polymer degradation was evaluated by characterizing polymer discs implanted in subcutaneous tissue of rats over a 56 day time period. Copolymers with the highest ratio of trimellitylimidoglycine in the polymer backbone were completely degraded by 56 days, the other compositions remained in the tissue as solid pellets at this time. In vivo degradation was much slower than the corresponding in vitro degradation.

scholarly journals C-Reactive Protein Adversely Alters the Protein–Protein Interaction of the Endothelial Isoform of Nitric Oxide Synthase

2010 ◽  
Vol 56 (8) ◽  
pp. 1345-1348 ◽  
Author(s):  
Simona Valleggi ◽  
Sridevi Devaraj ◽  
Mohan R Dasu ◽  
Ishwarlal Jialal
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Protein Interactions ◽  
Heat Shock Protein 90 ◽  
C Reactive Protein ◽  
Caveolin 1 ◽  
Reactive Protein ◽  
Oxide Synthase

BACKGROUND C-reactive protein (CRP) inhibits the activity of the endothelial isoform of nitric oxide synthase (eNOS) via uncoupling of the enzyme both in vitro and in vivo. eNOS activity appears to be related in part to its interaction with other cellular proteins, including heat shock protein 90 (Hsp90), caveolin-1, and porin. In this study, we examined the effect of CRP treatment of human aortic endothelial cells (HAECs) on eNOS interaction with caveolin-1, Hsp90, and porin. METHODS We incubated HAECs with CRP (0, 12.5, and 25 mg/L) for 1, 6, or 24 h and assessed the interaction of these proteins with eNOS by immunoprecipitation and western blotting. RESULTS CRP treatment (12.5 and 25 mg/L) of HAECs for 24 h significantly increased eNOS binding to caveolin-1 (40% and 54% increase, respectively; P < 0.05) and decreased binding to Hsp90 (33% and 66% decrease, respectively; P < 0.05). CRP (25 mg/L) also significantly decreased the binding of porin to eNOS (11% decrease, P < 0.05). Similar results were seen when HAECs were treated with CRP for 6 h. CONCLUSIONS These negative protein–protein interactions of eNOS were able to partly explain the CRP-induced decreases in the activity of this critical enzyme, which caused endothelial dysfunction.

scholarly journals In Vivo Simulation of Magnesium Degradability Using a New Fluid Dynamic Bench Testing Approach

2019 ◽  
Vol 20 (19) ◽  
pp. 4859 ◽  
Author(s):  
Ole Jung ◽  
Dario Porchetta ◽  
Marie-Luise Schroeder ◽  
Martin Klein ◽  
Nils Wegner ◽  
...  
Keyword(s):  
Degradation Rate ◽  
Test Bench ◽  
Fluid Dynamic ◽  
Dynamic Test ◽  
Gas Production ◽  
Hydrogen Gas ◽  
Human Blood Plasma ◽  
Degradation Rates

The degradation rate of magnesium (Mg) alloys is a key parameter to develop Mg-based biomaterials and ensure in vivo-mechanical stability as well as to minimize hydrogen gas production, which otherwise can lead to adverse effects in clinical applications. However, in vitro and in vivo results of the same material often differ largely. In the present study, a dynamic test bench with several single bioreactor cells was constructed to measure the volume of hydrogen gas which evolves during magnesium degradation to indicate the degradation rate in vivo. Degradation medium comparable with human blood plasma was used to simulate body fluids. The media was pumped through the different bioreactor cells under a constant flow rate and 37 °C to simulate physiological conditions. A total of three different Mg groups were successively tested: Mg WE43, and two different WE43 plasma electrolytically oxidized (PEO) variants. The results were compared with other methods to detect magnesium degradation (pH, potentiodynamic polarization (PDP), cytocompatibility, SEM (scanning electron microscopy)). The non-ceramized specimens showed the highest degradation rates and vast standard deviations. In contrast, the two PEO samples demonstrated reduced degradation rates with diminished standard deviation. The pH values showed above-average constant levels between 7.4–7.7, likely due to the constant exchange of the fluids. SEM revealed severe cracks on the surface of WE43 after degradation, whereas the ceramized surfaces showed significantly decreased signs of corrosion. PDP results confirmed the improved corrosion resistance of both PEO samples. While WE43 showed slight toxicity in vitro, satisfactory cytocompatibility was achieved for the PEO test samples. In summary, the dynamic test bench constructed in this study enables reliable and simple measurement of Mg degradation to simulate the in vivo environment. Furthermore, PEO treatment of magnesium is a promising method to adjust magnesium degradation.

scholarly journals Mg-Zn-Ca Alloys for Hemostasis Clips for Vessel Ligation: In Vitro and In Vivo Studies of Their Degradation and Response

Materials ◽  
2020 ◽  
Vol 13 (13) ◽  
pp. 3039 ◽  
Author(s):  
Yen-Hao Chang ◽  
Chun Chieh Tseng ◽  
Chih-Yeh Chao ◽  
Chung-Hwan Chen ◽  
Sung-Yen Lin ◽  
...  
Keyword(s):  
Degradation Rate ◽  
Protective Layer ◽  
Dip Coating ◽  
In Vivo Studies ◽  
Surface Measurement ◽  
In Vivo Experiments ◽  
Degradation Rates ◽  
And Behavior

To control the degradation rate of magnesium (Mg) alloys, chitosan (CHI) and L-glutamic acid (LGA) were used as coatings on Mg-Zn-Ca alloys via dip coating. In this study, either two or seven CHI/LGA layers were applied as a coating on Mg-2.8Zn-0.8Ca alloy (ZX31) and Mg-2.8Zn-0.8Ca hemostasis clips (ZX31 clips). The morphologies, compositions, and surface roughness of the specimens were characterized via scanning electron microscopy, Fourier transform infrared spectroscopy, and surface measurement devices. The degradation rates and behavior of the specimens were evaluated by immersing them in simulated body fluids and by applying these ZX31 clips on rabbits’ uterine tubes for five weeks. The specimen with seven layers (ZX31(CHI/LGA)7) exhibited improved corrosion behavior when compared with ZX31 or ZX31(CHI/LGA)2, with a reduced degradation rate of the Mg alloy in a simulated body environment. In vivo experiments showed that ZX31 clips exhibited good biocompatibilities in each group but could not maintain the clamping function for five weeks. The weight loss of ZX31(CHI/LGA)7 was significantly lower than that of the other groups. Consequently, it was verified that CHI can be used as a protective layer on a magnesium alloy surface via in vitro and in vivo experiments.

Discovery, in-vitro and in-vivo efficacy of an anti-inflammatory small molecule inhibitor of C-reactive protein

2021 ◽  
Author(s):  
Johannes Zeller ◽  
Karen Cheung Tung Shing ◽  
Tracy Nero ◽  
Guy Krippner ◽  
James McFadyen ◽  
...  
Keyword(s):  
Cell Activation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Acute Ischemia ◽  
C Reactive Protein ◽  
Endothelial Cell Activation ◽  
Reactive Protein ◽  
Anti Inflammatory

Abstract C-reactive protein (CRP) is an acute phase protein. We recently identified a novel mechanism that leads to a conformational change from the native, pentameric structure (pCRP) to a pentameric intermediate (pCRP*) and ultimately to the monomeric form, mCRP, both being highly pro-inflammatory. This ‘CRP activation’ is mediated by binding of pCRP to activated/damaged cell membranes via exposed phosphocholine (PC) lipid head groups. We designed a low molecular weight pCRP – PC inhibitor, C10M. Binding assays and X-ray crystallography revealed direct, competitive binding of C10M to pCRP, blocking interaction with PC and thereby inhibiting formation of pCRP*/mCRP and their pro-inflammatory effects. The anti-inflammatory potential of C10M was confirmed in-vitro by various measures of leukocyte and endothelial cell activation and in-vivo in rat models of acute ischemia/reperfusion injury and hindlimb transplantation. In conclusion, inhibition of pCRP*/mCRP generation via the PC-mimicking compound C10M represents a promising, potentially broadly applicable anti-inflammatory therapy.

scholarly journals C-Reactive Protein Stimulates Myeloperoxidase Release from Polymorphonuclear Cells and Monocytes: Implications for Acute Coronary Syndromes

2009 ◽  
Vol 55 (2) ◽  
pp. 361-364 ◽  
Author(s):  
Uma Singh ◽  
Sridevi Devaraj ◽  
Ishwarlal Jialal
Keyword(s):  
Plaque Rupture ◽  
Polymorphonuclear Cells ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Coronary Syndrome ◽  
Coronary Syndromes ◽  
Human Pmns ◽  
Poor Outcomes

Abstract Background: C-reactive protein (CRP), the prototypic marker of inflammation, is present in atherosclerotic plaques and appears to promote atherogenesis. Also, CRP has been localized to monocytes and tissue macrophages, which are present in the necrotic core of lesions prone to plaque rupture. Leukocyte-derived myeloperoxidase (MPO), primarily hosted in human polymorphonuclear cells (PMNs), has also been shown to be present in human atherosclerotic lesions. Because MPO and CRP concentrations are increased in acute coronary syndrome (ACS) patients and predict poor outcomes, we tested the effect of CRP on MPO release from PMNs and monocytes. Methods: We treated human PMNs and monocytes with CRP (25 and 50 mg/L for 6 h) and measured MPO release as total mass and activity in culture supernatants. We also measured nitro-tyrosinylation (NO2-Tyr) of LDL as an indicator of biological activity of CRP-mediated MPO release. Furthermore, we explored the effect of human CRP on MPO release in the rat sterile pouch model. Results: CRP treatment significantly increased release of MPO (both mass and activity) from human PMNs as well as monocytes (P < 0.05) and caused NO2-Tyr of LDL. Human CRP injection in rats resulted in increased concentrations of MPO in pouch exudates (P < 0.05), thus confirming our in vitro data. Conclusions: CRP stimulates MPO release both in vitro and in vivo, providing further cogent data for the proinflammatory effect of CRP. These results might further support the role of CRP in ACS.

scholarly journals C-Reactive Protein Induces Release of Both Endothelial Microparticles and Circulating Endothelial Cells In Vitro and In Vivo: Further Evidence of Endothelial Dysfunction

2011 ◽  
Vol 57 (12) ◽  
pp. 1757-1761 ◽  
Author(s):  
Sridevi Devaraj ◽  
Pappanaicken R Kumaresan ◽  
Ishwarlal Jialal
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Oxidized Ldl ◽  
Circulating Endothelial Cells ◽  
Early Event ◽  
C Reactive Protein ◽  
Endothelial Microparticles ◽  
Reactive Protein

BACKGROUND Inflammation is pivotal in atherosclerosis. A key early event in atherosclerosis is endothelial dysfunction. C-reactive protein (CRP), the prototypic marker of inflammation in humans, is a risk marker for cardiovascular disease, and there is mounting evidence to support its role in atherothrombosis. CRP has been shown to promote endothelial dysfunction both in vitro and in vivo. Emerging biomarkers of endothelial dysfunction include circulating endothelial cells (CECs) and endothelial microparticles (EMPs). However, there is a paucity of data examining the effect of CRP on CEC and EMP production in vitro and in vivo. METHODS In this report, we treated human aortic endothelial cells (HAECs) with increasing concentrations of CRP (0–50 μg/mL) or boiled CRP. We counted CECs and EMPs by flow cytometry. RESULTS Although CRP treatment resulted in a significant increase in release of both CECs and EMPs, boiled CRP failed to have an effect. Pretreatment of HAECs with sepiapterin or diethylenetriamine NONOate, both of which preserve nitric oxide (NO), resulted in attenuation of CRP's effects on CECs and EMPs. CD32 and CD64 blocking antibodies but not CD16 antibody or lectin-like oxidized LDL receptor 1 small interfering RNA (LOX-1 siRNA) prevented CRP-induced production of CECs and EMPs. Furthermore, delivery of human CRP to Wistar rats compared with human serum albumin resulted in significantly increased CECs and EMPs, corroborating the in vitro findings. CONCLUSIONS We provide novel data that CRP, via NO deficiency, promotes endothelial dysfunction by inducing release of CECs and EMPs, which are biomarkers of endothelial dysfunction.

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