scholarly journals Osseointegration of Alkali-Modified NANOZR Implants: An In Vivo Study

2019 ◽  
Vol 20 (4) ◽  
pp. 842 ◽  
Author(s):  
Satoshi Komasa ◽  
Mariko Nishizaki ◽  
Honghao Zhang ◽  
Seiji Takao ◽  
Derong Yin ◽  
...  

Ingredients and surface modification methods are being continually developed to improve osseointegration of dental implants and reduce healing times. In this study, we demonstrate in vitro that, by applying concentrated alkali treatment to NANOZR with strong bending strength and fracture toughness, a significant improvement in the bone differentiation of rat bone marrow cells can be achieved. We investigated the influence of materials modified with this treatment in vivo, on implanted surrounding tissues using polychrome sequential fluorescent labeling and micro-computer tomography scanning. NANOZR implant screws in the alkali-treated group and the untreated group were evaluated after implantation in the femur of Sprague–Dawley male rats, indicating that the amount of new bone in the alkali-modified NANOZR was higher than that of unmodified NANOZR. Alkali-modified NANOZR implants proved to be useful for the creation of new implant materials.

2021 ◽  
Vol 30 ◽  
pp. 096368972110354
Author(s):  
Eun-Jung Yoon ◽  
Hye Rim Seong ◽  
Jangbeen Kyung ◽  
Dajeong Kim ◽  
Sangryong Park ◽  
...  

Stamina-enhancing effects of human adipose derived stem cells (hADSCs) were investigated in young Sprague-Dawley rats. Ten-day-old male rats were transplanted intravenously (IV) or intracerebroventricularly (ICV) with hADSCs (1 × 106 cells/rat), and physical activity was measured by locomotor activity and rota-rod performance at post-natal day (PND) 14, 20, 30, and 40, as well as a forced swimming test at PND 41. hADSCs injection increased the moving time in locomotor activity, the latency in rota-rod performance, and the maximum swimming time. For the improvement of physical activity, ICV transplantation was superior to IV injection. In biochemical analyses, ICV transplantation of hADSCs markedly reduced serum creatine phosphokinase, lactate dehydrogenase, alanine transaminase, and muscular lipid peroxidation, the markers for muscular and hepatic injuries, despite the reduction in muscular glycogen and serum triglycerides as energy sources. Notably, hADSCs secreted brain-derived neurotrophic factor (BDNF) and nerve growth factor in vitro, and increased the level of BDNF in the brain and muscles in vivo. The results indicate that hADSCs enhance physical activity including stamina not only by attenuating tissue injury, but also by strengthening the muscles via production of BDNF.


2012 ◽  
Vol 112 (10) ◽  
pp. 1659-1669 ◽  
Author(s):  
Asaf Stein ◽  
Zhengkuan Mao ◽  
Joanna P. Morrison ◽  
Michelle V. Fanucchi ◽  
Edward M. Postlethwait ◽  
...  

Low concentrations of inhaled hydrogen sulfide (H2S) induce hypometabolism in mice. Biological effects of H2S in in vitro systems are augmented by lowering O2 tension. Based on this, we hypothesized that reduced O2 tension would increase H2S-mediated hypometabolism in vivo. To test this, male Sprague-Dawley rats were exposed to 80 ppm H2S at 21% O2 or 10.5% O2 for 6 h followed by 1 h recovery at room air. Rats exposed to H2S in 10.5% O2 had significantly decreased body temperature and respiration compared with preexposure levels. Heart rate was decreased by H2S administered under both O2 levels and did not return to preexposure levels after 1 h recovery. Inhaled H2S caused epithelial exfoliation in the lungs and increased plasma creatine kinase-MB activity. The effect of inhaled H2S on prosurvival signaling was also measured in heart and liver. H2S in 21% O2 increased Akt-PSer473 and GSK-3β-PSer9 in the heart whereas phosphorylation was decreased by H2S in 10.5% O2, indicating O2 dependence in regulating cardiac signaling pathways. Inhaled H2S and low O2 had no effect on liver Akt. In summary, we found that lower O2 was needed for H2S-dependent hypometabolism in rats compared with previous findings in mice. This highlights the possibility of species differences in physiological responses to H2S. Inhaled H2S exposure also caused tissue injury to the lung and heart, which raises concerns about the therapeutic safety of inhaled H2S. In conclusion, these findings demonstrate the importance of O2 in influencing physiological and signaling effects of H2S in mammalian systems.


2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Qian Wang ◽  
Xin Sui ◽  
Rui Chen ◽  
Pei-Yong Ma ◽  
Yong-Liang Teng ◽  
...  

Angiotensin (Ang) II contributes to the formation and development of myocardial fibrosis. Ghrelin, a gut peptide, has demonstrated beneficial effects against cardiovascular disease. In the present study, we explored the effect and related mechanism of Ghrelin on myocardial fibrosis in Ang II-infused rats. Adult Sprague-Dawley (SD) rats were divided into 6 groups: Control, Ang II (200ng/kg/min, microinfusion), Ang II+Ghrelin (100μg/kg, subcutaneously twice daily), Ang II+Ghrelin+GW9662 (a specific PPAR-γinhibitor, 1 mg/kg/d, orally), Ang II+GW9662, and Ghrelin for 4 wks. In vitro, adult rat cardiac fibroblasts (CFs) were pretreated with or without Ghrelin, Ghrelin+GW9662, or anti-Transforming growth factor (TGF)-β1 antibody and then stimulated with or without Ang II (100 nmol/L) for 24 h. Ang II infusion significantly increased myocardial fibrosis, expression of collagen I, collagen III, and TGF-β1, as well as TGF-β1 downstream proteins p-Smad2, p-Smad3, TRAF6, and p-TAK1 (all p<0.05). Ghrelin attenuated these effects. Similar results were seen in Ang II-stimulated rat cardiac fibroblasts in vitro. In addition, Ghrelin upregulated PPAR-γexpressionin vivoandin vitro, and treatment with GW9662 counteracted the effects of Ghrelin. In conclusion, Ghrelin ameliorated Ang II-induced myocardial fibrosis by upregulating PPAR-γand in turn inhibiting TGF-β1signaling.


2008 ◽  
Vol 82 (10) ◽  
pp. 739-747 ◽  
Author(s):  
Jean-Paul Payan ◽  
Michel Lafontaine ◽  
Patrice Simon ◽  
Fabrice Marquet ◽  
Catherine Champmartin-Gendre ◽  
...  

Toxicology ◽  
2016 ◽  
Vol 373 ◽  
pp. 41-53 ◽  
Author(s):  
Wenting Huang ◽  
Chao Quan ◽  
Peng Duan ◽  
Sha Tang ◽  
Wei Chen ◽  
...  

2020 ◽  
Vol 99 (5) ◽  
pp. 552-560 ◽  
Author(s):  
J. Watanabe ◽  
K. Sakai ◽  
Y. Urata ◽  
N. Toyama ◽  
E. Nakamichi ◽  
...  

Extracellular vesicles (EVs), several tens to hundreds of nanometers in size, are vesicles secreted by cells for intercellular communication. EVs released from mesenchymal stem cells (MSC-EVs) have the potential to treat multiple diseases. This study aimed to determine the effects of MSC-EVs on bisphosphonate-related osteonecrosis of the jaw (BRONJ), whose pathogenesis and treatment are not yet established. To this end, zoledronic acid (ZOL) was administered to bone marrow cells and fibroblasts in vitro. In vivo, a BRONJ model was produced by administering ZOL to rats and extracting teeth. Each MSC-EV-treated and nontreated group was compared histologically and molecularly. In vitro, the nontreated group showed an increased number of β-galactosidase-positive cells and expression of senescence-associated genes p21, pRB and senescence-related inflammatory cytokines. Conversely, MSC-EV administration decreased the number of senescent cells and expression levels of p21, pRB and inflammatory cytokines. In vivo, in the nontreated group, the socket was partially uncovered by the oral epithelium, leaving an exposed bone. Conversely, in the MSC-EV-treated group, the socket was healed. Besides, in the nontreated group, β-galactosidase-positive cells existed in the socket and colocalized with the CD90 and periostin-positive cells. However, there were few β-galactosidase-positive cells in the MSC-EV-treated group. Furthermore, gene expression of stem cell markers Bmi1 and Hmga2 and the vascular endothelial marker VEGF was significantly increased in the MSC-EV-treated group, compared with that in the nontreated group. These results indicate that MSC-EVs prevent ZOL-induced senescence in stem cells, osteoblasts, and fibroblasts and reduce inflammatory cytokines. Furthermore, administration of MSC-EVs prevented senescence of cells involved in wound healing and the spread of chronic inflammation around senescent cells, thereby promoting angiogenesis and bone regeneration and preventing BRONJ.


Endocrinology ◽  
2015 ◽  
Vol 156 (5) ◽  
pp. 1739-1749 ◽  
Author(s):  
Kelly E. Henry ◽  
Clinton T. Elfers ◽  
Rachael M. Burke ◽  
Oleg G. Chepurny ◽  
George G. Holz ◽  
...  

Challenges to peptide-based therapies include rapid clearance, ready degradation by hydrolysis/proteolysis, and poor intestinal uptake and/or a need for blood brain barrier transport. This work evaluates the efficacy of conjugation of vitamin B12 (B12) on sc administered peptide tyrosine tyrosine (PYY)3–36 function. In the current experiments, a B12-PYY3–36 conjugate was tested against native PYY3–36, and an inactive conjugate B12-PYYC36 (null control) in vitro and in vivo. In vitro experiments demonstrated similar agonism for the neuropeptide Y2 receptor by the B12-PYY3–36 conjugate (EC50 26.5 nM) compared with native PYY3–36 (EC50 16.0 nM), with the null control having an EC50 of 1.8 μM. In vivo experiments were performed in young adult male Sprague Dawley rats (9 wk). Daily treatments were delivered sc in five 1-hour pulses, each pulse delivering 5–10 nmol/kg, by implanted microinfusion pumps. Increases in hindbrain Fos expression were comparable 90 minutes after B12-PYY3–36 or PYY3–36 injection relative to saline or B12-PYYC36. Food intake was reduced during a 5-day treatment for both B12-PYY3–36- (24%, P = .001) and PYY3–36-(13%, P = .008) treated groups relative to baseline. In addition, reduction of food intake after the three dark cycle treatment pulses was more consistent with B12-PYY3–36 treatment (−26%, −29%, −27%) compared with the PYY3–36 treatment (−3%, −21%, −16%), and B12-PYY3–36 generated a significantly longer inhibition of food intake vs PYY3–36 treatment after the first two pulses (P = .041 and P = .036, respectively). These findings demonstrate a stronger, more consistent, and longer inhibition of food intake after the pulses of B12-PYY3–36 conjugate compared with the native PYY3–36.


2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Xiang Zheng ◽  
Jian Wen ◽  
Teng-hui Liu ◽  
Qiu-Geng Ou-yang ◽  
Jian-ping Cai ◽  
...  

Objective. To discuss the effects of genistein on the metabolism of celecoxib in vitro and in vivo. Method. In vitro, the effects of genistein on the metabolism of celecoxib were studied using rat and human liver microsomes. In vivo, pharmacokinetics of celecoxib was evaluated in rats with or without genistein. Fifteen Sprague-Dawley (SD) rats were randomized into three groups: celecoxib (A group), celecoxib and 50 mg/kg genistein (B group), and celecoxib and 100 mg/kg genistein (C group). Single dose of 33.3 mg/kg celecoxib was orally administered 30 min after genistein ig. At 0.5, 1, 2, 3, 4, 6, 8, 10, 12, and 24 h after celecoxib administration, 300–400 µl blood samples were collected and the concentration of celecoxib was analyzed by ultrahigh-performance liquid chromatography-tandem mass spectrometry system. Result. Genistein showed notable inhibitory effects on three microsomes. It affected pharmacokinetics of celecoxib in vivo experiments. Genistein had dramatically ability to suppress CYP2C9∗1 and ∗3. After pretreatment with genistein, AUC and Cmax of the C group were higher than B group. CLz/F of C group was lower than the B group. Conclusion. Genistein inhibits the conversion of celecoxib in vitro and in vivo. So, the dosage of celecoxib should be adjusted if it was used associated with genistein.


1987 ◽  
Vol 110 ◽  
Author(s):  
Haned A. Benghuzzi ◽  
Praphulla K. Bajpai

AbstractSprague-Dawley albino male rats (25) were divided into five groups consisting of five rats each. Polymer (polylactic acid) impregnated ALCAP capsules filled with 40 mg DFMO were implanted subcutaneously (SC) or intraperitoneally (IP) in Group I and II rats respectively. Rats in Group III were implanted with empty polymer impregnated ALCAP capsules (ALCAP control). Group IV rats were administered orally 3% DFMO in drinking water. Rats in Group V served as controls. Blood samples were collected every week for nine weeks via the tail artery. The concentration of DFNO in the plasma was determined. Data obtained showed that the levels of DFMO in the serum of rats in groups I, I, and IV were 64.71 ±4.08. 219.18 ± 14.48, 16.71 ± 5.21 ug ml−1, respectively at the end of nine weeks. Body weights of the controls and DFMO treated rats were not significantly different (p<0.05). The diarrhea often noted in rats treated orally with DFHO was not observed in rats implanted with ALCAP or ALCAP capsules filled with DFMO. The results of this study suggest that: (1) polymer impregnated ALCAP ceramic implants can be used to deliver DFMO in vivo in a sustained manner for long durations of time, and (2) a ceramic system can be designed to deliver DFNO and drugs such as DFMO in a sustained manner over long durations of time in humans.


Author(s):  
N.K.R. Smith ◽  
K.E. Hunter ◽  
P. Mobley ◽  
L.P. Felpel

Electron probe energy dispersive x-ray microanalysis (XRMA) offers a powerful tool for the determination of intracellular elemental content of biological tissue. However, preparation of the tissue specimen , particularly excitable central nervous system (CNS) tissue , for XRMA is rather difficult, as dissection of a sample from the intact organism frequently results in artefacts in elemental distribution. To circumvent the problems inherent in the in vivo preparation, we turned to an in vitro preparation of astrocytes grown in tissue culture. However, preparations of in vitro samples offer a new and unique set of problems. Generally, cultured cells, growing in monolayer, must be harvested by either mechanical or enzymatic procedures, resulting in variable degrees of damage to the cells and compromised intracel1ular elemental distribution. The ultimate objective is to process and analyze unperturbed cells. With the objective of sparing others from some of the same efforts, we are reporting the considerable difficulties we have encountered in attempting to prepare astrocytes for XRMA.Tissue cultures of astrocytes from newborn C57 mice or Sprague Dawley rats were prepared and cultured by standard techniques, usually in T25 flasks, except as noted differently on Cytodex beads or on gelatin. After different preparative procedures, all samples were frozen on brass pins in liquid propane, stored in liquid nitrogen, cryosectioned (0.1 μm), freeze dried, and microanalyzed as previously reported.


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