scholarly journals Effect and Mechanism of 808 nm Light Pretreatment of Hypoxic Primary Neurons

2014 ◽  
Vol 2014 ◽  
pp. 1-5
Author(s):  
Xin Chen ◽  
Qiang-Li Wang ◽  
Shuang Li ◽  
Xian-qiang Mi
Keyword(s):  
Cell Viability ◽  
Cortical Neurons ◽  
Colorimetric Assay ◽  
Neuronal Morphology ◽  
Light Irradiation ◽  
Control Group ◽  
Primary Neurons ◽  
Atp Content ◽  
Low Intensity ◽  
Primary Mouse

This study investigated the effect of low intensity 808 nm light pretreatment of hypoxic primary neurons. Cobalt chloride (CoCl2) has been used to induce hypoxic injury in primary mouse cortical neurons. Low intensity 808 nm light was from light-emitting diode (LED). Cells were randomly divided into 4 groups: normal control group, CoCl2-induced group, CoCl2-induced group with 808 nm light irradiation pretreatment, and normal group with 808 nm light irradiation pretreatment. Effect of low intensity 808 nm light on neuronal morphology has been observed by microscope. MTT colorimetric assay has been used to detect the effect of low intensity 808 nm light on neuronal activity. Adenosine triphosphate (ATP) concentration and cytochrome C oxidase (COX) activity has been detected to study the effect of low intensity 808 nm light on neuronal mitochondria function. The results indicated that low intensity 808 nm light pretreatment alone did not affect cell viability, COX activity, and ATP content of neurons and low intensity 808 nm light pretreatment promoted the cell viability, COX activity, and ATP content of neurons with CoCl2exposure; however, low intensity 808 nm light pretreatment did not completely recover COX activity and cellular ATP content of primary neurons with CoCl2exposure to the level of the normal neurons.

scholarly journals In Vitro Cytotoxicity Evaluation of Three Root-End Filling Materials in Human Periodontal Ligament Fibroblasts

2016 ◽  
Vol 27 (2) ◽  
pp. 187-191 ◽  
Author(s):  
Hernán Coaguila-Llerena ◽  
Abraham Vaisberg ◽  
Zulema Velásquez-Huamán
Keyword(s):  
Cell Viability ◽  
Periodontal Ligament ◽  
Colorimetric Assay ◽  
Control Group ◽  
Repair Material ◽  
Periodontal Ligament Fibroblasts ◽  
Filling Materials ◽  
Root Repair ◽  
Human Periodontal Ligament Fibroblasts

Abstract The aim of this study was to evaluate in vitro the cytotoxicity on human periodontal ligament fibroblasts of three root-end filling materials: MTA Angelus(r), EndoSequence Root Repair Material Putty(r) and Super EBA(r). A primary culture of human periodontal ligament fibroblasts was previously obtained in order to evaluate the cytotoxicity of the three extracts from the root-end filling materials after 2 and 7 days of setting. Serial dilutions of these extracts (1:1, 1:2, 1:4 and 1:8) were evaluated at 1, 3 and 7 days using the methyl-thiazol-tetrazolium (MTT) colorimetric assay. Cell viability was evaluated as percentage of the negative control group, which represented 100% cell viability. Statistical analyses were done with t-test, ANOVA and Kruskal-Wallis test at a significance level of 5%. It was found that the main difference among root-end filling materials was in the higher dilutions (p<0.05), but there was a similar behavior in lower dilutions (p>0.05). Cell viability of MTA Angelus(r) was superior for 2-day setting (p<0.05), compared with the other two root-end fillings. There were no statistically significant differences between 7-day set MTA Angelus(r) and EndoSequence Root Repair Material Putty(r). Super EBA(r) showed the lowest percentage of cell viability at higher dilutions (p<0.05). Therefore, MTA Angelus(r) and EndoSequence Root Repair Material Putty(r) were less cytotoxic in the highest dilution (1:1) compared with Super EBA(r).

scholarly journals The protective effects of melatonin in high glucose environment by alleviating autophagy and apoptosis on primary cortical neurons

2021 ◽  
Author(s):  
Xiong Lijiao ◽  
Song Liu ◽  
Chaoming Liu ◽  
Tianting Guo ◽  
Zhihua Huang ◽  
...  
Keyword(s):  
Protein Expression ◽  
Protective Effect ◽  
Cell Viability ◽  
High Glucose ◽  
Cortical Neurons ◽  
Neuroprotective Effect ◽  
Control Group ◽  
Primary Cortical Neurons ◽  
Apoptosis Rate ◽  
Glucose Group

Abstract Cognitive dysfunction has been regarded as a complication of diabetes. Melatonin shows a neuroprotective effect on various neurological diseases. However, it’s protective effect on cortical neurons in high glucose environment has not been reported. Our present study aims to observe the protective effect of melatonin on rat cortical neurons and its relationship with autophagy in high glucose environment. The rat primary cortical neurons damaged model was induced by high glucose. The CCK-8, flow cytometry, Western Blot and immunofluorescence methods were used to examine the cell viability, apoptosis rate and proteins expression. Our results showed that there were no differences in cell viability, apoptosis rate, and protein expression among the control MLT and mannitol group. The cell viability of the glucose group was significantly lower than that of the control group, and the apoptosis rate of the glucose group was significantly higher than that of the control group. Compared with the glucose group, the glucose + melatonin group showed a significant increase in cell viability and a notable decrease in apoptosis rate. Melatonin concentration of 0.1-1 mmol/L can significantly reduce the injury of cortical neurons by high glucose. Compared with the control group, the glucose group showed a significant reduction of Bcl-2 protein expression, while remarkable elevations of Bax, caspase-3, Beclin-1 and LC3B levels. The neurons pre-administered with melatonin obtained significantly reversed these changes induced by high glucose. The phosphorylation levels of Akt and mTOR in the glucose group were significantly lower than those in the control group, were significantly increased in the glucose + MLT group compared with the glucose group. These data indicated that melatonin has a neuroprotective effect on cortical neurons under high glucose environment, which may work by activating Akt/mTOR pathway and following the down-regulation of autophagy.

scholarly journals A microscopy-based small molecule screen in primary neurons reveals neuroprotective properties of the FDA-approved anti-viral drug Elvitegravir

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Simon F. Merz ◽  
C. Peter Bengtson ◽  
Clara Tepohl ◽  
Anna M. Hagenston ◽  
Hilmar Bading ◽  
...  
Keyword(s):  
Cell Death ◽  
Membrane Potential ◽  
Nmda Receptor ◽  
Mitochondrial Membrane Potential ◽  
Cortical Neurons ◽  
Mitochondrial Membrane ◽  
Glutamate Toxicity ◽  
Primary Neurons ◽  
Screening Assay ◽  
Primary Mouse

Abstract Glutamate toxicity is a pathomechanism that contributes to neuronal cell death in a wide range of acute and chronic neurodegenerative and neuroinflammatory diseases. Activation of the N-methyl-D-aspartate (NMDA)-type glutamate receptor and breakdown of the mitochondrial membrane potential are key events during glutamate toxicity. Due to its manifold functions in nervous system physiology, however, the NMDA receptor is not well suited as a drug target. To identify novel compounds that act downstream of toxic NMDA receptor signaling and can protect mitochondria from glutamate toxicity, we developed a cell viability screening assay in primary mouse cortical neurons. In a proof-of-principle screen we tested 146 natural products and 424 FDA-approved drugs for their ability to protect neurons against NMDA-induced cell death. We confirmed several known neuroprotective drugs that include Dutasteride, Enalapril, Finasteride, Haloperidol, and Oxybutynin, and we identified neuroprotective properties of Elvitegravir. Using live imaging of tetramethylrhodamine ethyl ester-labelled primary cortical neurons, we found that Elvitegravir, Dutasteride, and Oxybutynin attenuated the NMDA-induced breakdown of the mitochondrial membrane potential. Patch clamp electrophysiological recordings in NMDA receptor-expressing HEK293 cell lines and primary mouse hippocampal neurons revealed that Elvitegravir does not act at the NMDA receptor and does not affect the function of glutamatergic synapses. In summary, we have developed a cost-effective and easy-to-implement screening assay in primary neurons and identified Elvitegravir as a neuro- and mitoprotective drug that acts downstream of the NMDA receptor.

Abstract WMP35: Low Level Laser Therapy (LLLT) Protects Against Oxygen-Glucose Deprivation-Induced Neuron Death by Modulating Nitric Oxide and ROS Production In Vitro

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Zhanyang Yu ◽  
Ning Liu ◽  
Yadan Li ◽  
Jianhua Zhao ◽  
Eng H Lo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Cell Survival ◽  
Cortical Neurons ◽  
Post Treatment ◽  
Low Level Laser Therapy ◽  
Primary Neurons ◽  
Ros Production ◽  
Primary Mouse ◽  
Survival Signaling

Background: LLLT has been shown to be neurorprotective against cerebral ischemia in animals. Initial human clinical trials demonstrated safety and potential beneficial profiles. A pivotal clinical trial with TLT is ongoing for ischemic stroke. However, the underlying neuroprotective mechanisms require further definition. We previously showed LLLT protected primary neurons against OGD. In the current study, we tested the hypothesis that LLLT may attenuate OGD-induced nitric oxide (NO) and ROS production and associated cell survival signaling, causing reduced cell death in primary mouse cortical neurons. Method: At day 8 of culture, neurons were subjected to 4 hr OGD. LLLT was applied at 2 hr reoxygenation. NO level, nNOS expression, ROS level, and cell survival signaling were measured post-LLLT. Cell death was measured at 20 hr after OGD. Results were expressed as fold of normal control, mean ± SEM, n = 3-5 per group, P <0.05 was considered statistically significant. Results: OGD significantly increased NO level in primary neurons (2.12 ± 0.47, 2.67 ± 1.07, and 2 ± 0.77 at 5 min, 30 min and 1 hr post-treatment, respectively), but the increase was significantly reduced by LLLT (1.08 ± 0.44 at 5 min and 1.45 ± 0.73 at 30 min post-LLLT). OGD also significantly increased nNOS mRNA level (2.17 ± 0.42, 3.99 ± 1.7, and 2.60 ± 0.7 at 5 min, 30 min and 1 hr post-treatment, respectively), while the increase was significantly ameliorated by LLLT (0.50 ± 0.08 at 30 min and 0.34 ± 0.45 at 1 hr post-LLLT). Additionally, 50 uM NO donor SNAP exposure for 48 hr induced 23.6 ± 2.5% cell death, which was significantly ameliorated by LLLT (12.3 ± 4.2% cell death), indicating LLLT may directly protect NO-mediated neurotoxicity. Furthermore, LLLT significantly reduced OGD-induced ROS production at 5 min, 30 min and 1 hr post-LLLT. Finally, OGD suppressed neuron survival signaling p-Akt and Bcl-2 protein expressions, but they were significantly rescued by LLLT. Conclusion: These results suggest LLLT protection against OGD may be partially through reducing OGD-induced NO and ROS production, and restoring OGD-suppressed cell survival signaling.

scholarly journals CBIO-07. CELL DEATH INDUCED BY AN OSCILLATING MAGNETIC FIELD IN PATIENT DERIVED GLIOBLASTOMA CELLS IS MEDIATED BY REACTIVE OXYGEN SPECIES

2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii17-ii17
Author(s):  
Shashank Hambarde ◽  
Martyn Sharpe ◽  
David Baskin ◽  
Santosh Helekar
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cell Viability ◽  
Cortical Neurons ◽  
Reactive Oxygen ◽  
Great Promise ◽  
Antioxidant Vitamin ◽  
Ros Generation ◽  
Oxygen Species ◽  
Novel Therapy

Abstract Noninvasive cancer therapy with minimal side effects would be ideal for improving patient outcome in the clinic. We have developed a novel therapy using strong rotating magnets mounted on a helmet. They generate oscillating magnetic fields (OMF) that penetrate through the skull and cover the entire brain. We have demonstrated that OMF can effectively kill patient derived glioblastoma (GBM) cells in cell culture without having cytotoxic effects on cortical neurons and normal human astrocytes (NHA). Exposure of GBM cells to OMF reduced the cell viability by 33% in comparison to sham-treated cells (p&lt; 0.001), while not affecting NHA cell viability. Time lapse video-microscopy for 16 h after OMF exposure showed a marked elevation of mitochondrial reactive oxygen species (ROS), and rapid apoptosis of GBM cells due to activation of caspase 3. Addition of a potent antioxidant vitamin E analog Trolox effectively blocked OMF-induced GBM cell death. Furthermore, OMF significantly potentiated the cytotoxic effect of the pro-oxidant Benzylamine. The results of our studies demonstrate that OMF-induced cell death is mediated by ROS generation. These results demonstrate a potent oncolytic effect on GBM cells that is novel and unrelated to any previously described therapy, including a very different mechanism of action and different technology compared to Optune therapy. The effect is very powerful, and unlike Optune, can be seen within hours after initiation of treatment. We believe that this technology holds great promise for new, effective and nontoxic treatment of glioblastoma.

scholarly journals Cytotoxicity assessment of different doses of ozonated water on dental pulp cells

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ferdiye Küçük ◽  
Sibel Yıldırım ◽  
Serap Çetiner
Keyword(s):  
Cell Viability ◽  
Repeated Measures ◽  
Dental Pulp ◽  
Control Group ◽  
Dental Pulp Cells ◽  
Time Points ◽  
Significant Difference ◽  
Pulp Cells ◽  
Time Point ◽  
Ozonated Water

Abstract Background The purpose of this study was to assess the cytotoxicity of various concentrations of ozonated water (OW) on human primary dental pulp cells. Methods Human primary dental pulp cells were isolated from exfoliated primary canine teeth of an 11-year-old patient with good systemic and oral health. Afterwards, cells were divided into 6 experimental groups; four groups of OW in concentrations of 2 mg/L, 4 mg/L, 8 mg/L, and 16 mg/L, untreated control group, and cell culture without cells. Cytotoxicity was evaluated after exposure for 5-min exposure using Mosmann’s Tetrazolium Toxicity (MTT) assay at 0 h and 48 h time points. Data were analyzed using a repeated measures analysis of variance and Post-hoc tests were performed using Bonferroni correction for multiple comparisons. Results All experimental groups showed proliferation at 0 h time point. However, all groups also experienced a decrease in overtime at 48 h time point (p < 0.05). At both time points 2 mg/L OW showed the highest cell viability as well as proliferation. At 0 h time point, the increase in cell viability for all experimental groups was found statistically significant when compared to positive control group (p < 0.05). At 48 h time point, although 8 mg/L and 16 mg/L OW showed statistically significant reduction in compare to 0 h time point, 2 mg/L and 4 mg/L OW groups didn’t experience any statistically significant difference (p < 0.05). Conclusion Considering our findings, due to ozonated water's induced a higher proliferation rate of dental pulp cells, indicating their biocompatibility and a possible adjuvant on irrigating agent in regenerative endodontic procedures.

scholarly journals Mitochondrial fission and mitophagy are independent mechanisms regulating ischemia/reperfusion injury in primary neurons

2021 ◽  
Vol 12 (5) ◽  
Author(s):  
Anthony R. Anzell ◽  
Garrett M. Fogo ◽  
Zoya Gurm ◽  
Sarita Raghunayakula ◽  
Joseph M. Wider ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Ischemia Reperfusion Injury ◽  
Mitochondrial Dynamics ◽  
Ischemia Reperfusion ◽  
Mitochondrial Fission ◽  
Conditional Knockout ◽  
Mitochondrial Morphology ◽  
Primary Neurons ◽  
Mitochondrial Fragmentation

AbstractMitochondrial dynamics and mitophagy are constitutive and complex systems that ensure a healthy mitochondrial network through the segregation and subsequent degradation of damaged mitochondria. Disruption of these systems can lead to mitochondrial dysfunction and has been established as a central mechanism of ischemia/reperfusion (I/R) injury. Emerging evidence suggests that mitochondrial dynamics and mitophagy are integrated systems; however, the role of this relationship in the context of I/R injury remains unclear. To investigate this concept, we utilized primary cortical neurons isolated from the novel dual-reporter mitochondrial quality control knockin mice (C57BL/6-Gt(ROSA)26Sortm1(CAG-mCherry/GFP)Ganl/J) with conditional knockout (KO) of Drp1 to investigate changes in mitochondrial dynamics and mitophagic flux during in vitro I/R injury. Mitochondrial dynamics was quantitatively measured in an unbiased manner using a machine learning mitochondrial morphology classification system, which consisted of four different classifications: network, unbranched, swollen, and punctate. Evaluation of mitochondrial morphology and mitophagic flux in primary neurons exposed to oxygen-glucose deprivation (OGD) and reoxygenation (OGD/R) revealed extensive mitochondrial fragmentation and swelling, together with a significant upregulation in mitophagic flux. Furthermore, the primary morphology of mitochondria undergoing mitophagy was classified as punctate. Colocalization using immunofluorescence as well as western blot analysis revealed that the PINK1/Parkin pathway of mitophagy was activated following OGD/R. Conditional KO of Drp1 prevented mitochondrial fragmentation and swelling following OGD/R but did not alter mitophagic flux. These data provide novel evidence that Drp1 plays a causal role in the progression of I/R injury, but mitophagy does not require Drp1-mediated mitochondrial fission.

scholarly journals Effect of intracellular uptake of nanoparticle-encapsulated trehalose on the hemocompatibility of allogeneic valves in the VS83 vitrification protocol

2020 ◽  
Vol 7 ◽  
pp. 184954352098317
Author(s):  
Balamurugan Vasudevan ◽  
Qing Chang ◽  
Bin Wang ◽  
Siyang Huang ◽  
Yulong Sui ◽  
...  
Keyword(s):  
Cell Viability ◽  
Heart Valves ◽  
Corn Starch ◽  
Colloidal Suspensions ◽  
Initial Step ◽  
Control Group ◽  
Hydroxyapatite Nanoparticles ◽  
Reticular Fibers ◽  
Terminal Complement ◽  
Ammonia Method

Trehalose is a disaccharide molecule consisting of two molecules of glucose. Industrially, trehalose is derived from corn starch and utilized as a drug. This study aims to examine whether the integration of nanoparticle-encapsulated trehalose to the Ice-Free Cryopreservation (IFC) method for preserving heart valves has better cell viability, benefits to protect the extracellular matrix (ECM), and reduce immune response after storage. For the experiment to be carried out, we obtained materials, and the procedures were carried out in the following manner. The initial step was the preparation of hydroxyapatite nanoparticles, followed by precipitation to acquire Apatite colloidal suspensions. Animals were obtained, and their tissue isolation and grouping were done ethically. All samples were then divided into four groups, Control group, Conventional Frozen Cryopreservation (CFC) group, IFC group, and IFC + T (IFC with the addition of 0.2 M nanoparticle-encapsulated Trehalose) group. Histological analysis was carried out via H&E staining, ECM components were stained with Modified Weigert staining, and the Gomori Ammonia method was used to stain reticular fibers. Alamar Blue assay was utilized to assess cell viability. Hemocompatibility was evaluated, and samples were processed for immunohistochemistry (TNFα and IL-10). Hemocompatibility was quantified using Terminal Complement Complex (TCC) and Neutrophil elastase (NE) as an indicator. The results of the H&E staining revealed less formation of extracellular ice crystals and intracellular vacuoles in the IFC + T group compared with all other groups. The CFC group’s cell viability showed better viability than the IFC group, but the highest viability was exhibited in the IFC + T group (70.96 ± 2.53, P < 0.0001, n = 6). In immunohistochemistry, TNFα levels were lowest in both IFC and IFC + T group, and IL-10 expression had significantly reduced in IFC and IFC + T group. The results suggested that the nanoparticle encapsulated trehalose did not show significant hemocompatibility issues on the cryopreserved heart valves.

Nrf2 mediates the neuroprotective effect of isoflurane preconditioning in cortical neuron injury induced by oxygen-glucose deprivation

2021 ◽  
pp. 096032712198941
Author(s):  
X-S Liu ◽  
X-L Bai ◽  
Z-X Wang ◽  
S-Y Xu ◽  
Y Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cortical Neuron ◽  
Cortical Neurons ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Lactate Dehydrogenase Activity ◽  
Primary Mouse ◽  
Ldh Release ◽  
Neuron Injury ◽  
And Oxidative Stress

Objective: To investigate how nuclear factor-E2-related factor 2 (Nrf2) involved in the protective effect of isoflurane (Iso) preconditioning in oxygen glucose deprivation (OGD)-induced cortical neuron injury. Methods: Primary mouse cortical neurons were divided into Control, ML385 (an Nrf2 inhibitor), Iso, Iso + ML385, OGD, ML385 + OGD, Iso + OGD, and Iso + ML385 + OGD groups. Lactate dehydrogenase activity (LDH) release and oxidative stress indexes were quantified. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to detect cell viability, Annexin V-FITC/propidium iodide (PI) staining to measure cell apoptosis, dichloro-dihydro-fluorescein diacetate (DCFH-DA) method to test reactive oxygen species (ROS), and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and Western blotting to evaluate genes and protein expression. Results: Iso preconditioning reduced LDH release and inhibited cell cytotoxicity in OGD-induced cortical neurons, which was abolished by ML385. Iso preconditioning increased the Nrf2 nuclear translocation in cortical neurons. Meanwhile, Iso decreased the OGD-induced apoptosis with the down-regulations of Bax and Caspase-3 and the up-regulation of Bcl-2, which was reversed by ML385. OGD enhanced the level of ROS and malondialdehyde (MDA) in cortical neurons, but reduced the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), which were aggravated in ML385 + OGD group and mitigated in Iso + OGD group. No observable difference was found between OGD group and Iso + ML385 + OGD group regarding apoptosis-related proteins and oxidative stress-related indexes. Conclusion: Iso preconditioning up-regulated Nrf2 level to play its protective role in OGD-induced mouse cortical neuron injury.

scholarly journals Biological characterization of implant surfaces - in vitro study

2015 ◽  
Vol 44 (4) ◽  
pp. 195-199 ◽  
Author(s):  
Priscilla Barbosa Ferreira Soares ◽  
Camilla Christian Gomes Moura ◽  
Huberth Alexandre da Rocha Júnior ◽  
Paula Dechichi ◽  
Darceny Zanetta-Barbosa
Keyword(s):  
Alkaline Phosphatase ◽  
Cell Viability ◽  
Total Protein ◽  
Cell Attachment ◽  
Control Group ◽  
Mitochondrial Activity ◽  
Serum Total Protein ◽  
Trypan Blue Exclusion ◽  
Experimental Surface

<title>Abstract</title><sec><title>Objective</title><p>Evaluate the biological performance of titanium alloys grade IV under different surface treatments: sandblasting and double etching (Experimental surface 1; Exp1, NEODENT); surface with wettability increase (Experimental surface 2; Exp2, NEODENT) on response of preliminary differentiation and cell maturation.</p></sec><sec><title>Material and method</title><p>Immortalized osteoblast cells were plated on Exp1 and Exp2 titanium discs. The polystyrene plate surface without disc was used as control group (C). Cell viability was assessed by measuring mitochondrial activity (MTT) at 4 and 24 h (n = 5), cell attachment was performed using trypan blue exclusion within 4 hours (n = 5), serum total protein and alkaline phosphatase normalization was performed at 4, 7 and 14 days (n = 5). Data were analyzed using one-way ANOVA and Tukey test.</p></sec><sec><title>Result</title><p>The values of cell viability were: 4h: C– 0.32±0.01<sup>A</sup>; Exp1– 0.34±0.08<sup>A</sup>; Exp2– 0.29±0.03<sup>A</sup>. 24h: C– 0.43±0.02<sup>A</sup>; Exp1– 0.39±0.01<sup>A</sup>; Exp2– 0.37±0.03<sup>A</sup>. The cell adhesion counting was: C– 85±10<sup>A</sup>; Exp1- 35±5<sup>B</sup>; Exp2– 20±2<sup>B</sup>. The amounts of serum total protein were 4d: C– 40±2<sup>B</sup>; Exp1– 120±10<sup>A</sup>; Exp2– 130±20<sup>A</sup>. 7d: C– 38±2<sup>B</sup>; Exp1– 75±4<sup>A</sup>; Exp2– 70±6<sup>A</sup>. 14 d: C– 100±3<sup>A</sup>; Exp1– 130±5<sup>A</sup>; Exp2– 137±9<sup>A</sup>. The values of alkaline phosphatase normalization were: 4d: C– 2.0±0.1<sup>C</sup>; Exp1– 5.1±0.8<sup>B</sup>; Exp2– 9.8±2.0<sup>A</sup>. 7d: C– 1.0±0.01<sup>C</sup>; Exp1– 5.3±0.5<sup>A</sup>; Exp2– 3.0±0.3<sup>B</sup>. 14 d: C– 4.1±0.3<sup>A</sup>; Exp1– 4.4±0.8<sup>A</sup>; Exp2– 2.2±0.2<sup>B</sup>. Different letters related to statistical differences.</p></sec><sec><title>Conclusion</title><p>The surfaces tested exhibit different behavior at dosage of alkaline phosphatase normalization showing that the Exp2 is more associated with induction of cell differentiation process and that Exp1 is more related to the mineralization process.</p></sec>

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