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treatment with Al3+ at a concentration range of 10-7-10-5 M in the cultures of both MOB and AOB. The stimulatory effects of Al3+ on the differentiation markers were abolished by the pretreatment of the cells with pertussis toxin (PTX), an inhibitor of Gi protein, indicating that the effects of Al3+ are mediated through a receptor coupled with Gi pr...
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... manner as well as a paracrine manner, Al 3+ may regulate differentiation and proliferation of MOB and AOB by affecting the rate of PGE 2 secretion from these cells. It is, how- ever, not likely because no significant change was observed in the amount of PGE 2 secreted into the medium after the treatment with various concentra- tions of Al 3+ (Fig. 2). Figure 3 shows the effect of Al 3+ on the markers for differentiation and proliferation of osteoblasts in the presence of 10 -6 M 17-phenyl-ω-trinor-PGE 2 , a selective EP 1 agonist, in the cultures of MOB and AOB. In the absence of Al 3+ , the EP 1 agonist in- creased all markers for differentiation by 70 to 80% and decreased [ 3 ...
Citations
... Si ions exhibit antioxidant activity and enhance bone formation [31]. F ions stimulate osteoprogenitor cells [32] and Al ions trigger bone nodule formation [33], and the combination of F and Al ions has been reported to enhance the proliferation and differentiation of human pulp cells without toxicity [18]. Meanwhile, there are various reports on the toxicity of these ions, especially F [34]. ...
The effects of surface pre‐reacted glass‐ionomer (S‐PRG) filler on pulpal cells and on the composition of dentinal deposits were investigated. Proliferation (CCK‐8), cytotoxicity (LDH), and differentiation activity (ALP) tests, along with cell morphology observations, were conducted at 6 and 24 h after treatment of pulpal cells with different S‐PRG filler eluate concentrations. Dentinal surfaces were immersed in deionized water or S‐PRG filler eluate followed by immersion in deionized water or simulated body fluid and observed under scanning electron microscope and elemental analysis using energy dispersive x‐ray spectrometer. At 24 h, there were significant differences in CCK‐8 and ALP activity values between the groups in a concentration‐dependent manner. LDH test data were not significantly different among the groups. Cell morphology was not altered at either exposure time. However, decreased cellular density was observed with the highest eluate concentration. Crystalline deposits and occluded dentinal tubules were observed in samples immersed in S‐PRG filler with a later immersion in simulated body fluid, which also showed higher concentrations of certain ions compared to surfaces that were not initially treated with S‐PRG filler. The lowest two eluate concentrations did not show significant toxicity. S‐PRG enhanced the effect of simulated body fluid in the formation of mineral deposits.
Surface reaction-type pre-reacted glass-ionomer (PRG) fillers have the ability to slowly release various ions. This study investigated the effects of cement-containing surface reaction-type PRG filler (PRG cement) on the viability and differentiation of human dental pulp cells derived from deciduous teeth (hDPC-Ds). Other materials generally used for pulp capping, Dycal and Fuji glass-ionomer cement Type II, were also tested by culturing hDPC-Ds with the extract of each material. The viability of hDPC-Ds was measured by methyl-thiazol-tetrazolium [3-(4, 5-di-methylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide] assay. Odontogenic differentiation of hDPC-Ds was evaluated by alkaline phosphatase (ALP) activity and immunocytochemistry. The concentration of each ion in the extract was assessed by ion pair chromatography, inductively coupled plasma, and fluoride ion meter. Based on the results of ion analysis, a medium containing fluoride (F) and aluminum (Al) ions was reconstituted. Human DPC-Ds were cultured in this medium, followed by 3-(4, 5-di-methylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assays and measurement of ALP activity. PRG cement extracts were found to significantly enhance the viability, ALP activity, ALP staining in the extracellular matrix of hDPC-Ds, and release of F and Al ions. These ions, in turn, enhanced the viability and differentiation of hDPC-Ds. Taken together, these results indicate that the proliferation and differentiation of hDPC-Ds was enhanced by PRG cement and that F and Al, which elute from the PRG filler, were most likely involved in the proliferation and differentiation of hDPC-Ds. These findings suggest that PRG cement is potentially useful as a pulp capping agent.
Objective: Ulcerative colitis (UC) may be characterized by metal ion and antioxidant deficiencies. Raphacol bile granule (containing vitamin A, E, C, polyphenols and isothiocyanates) supplementary treatment was applied in moderately active UC patients to estimate its effect on the element status. Materials and methods: Element content (Al, Ca, Cu, Fe, Mg, Mn, P, S and Zn) in erythrocyte of 15 Caucasian volunteers, 25 moderately UC patients with therapy recommended by WHO and 25 patients treated with Raphacol bile granule (0.2 g/d for 6 months) were studied with ICP-AES. Results and conclusions: Significantly decreased Ca, Fe and Zn concentrations were found in erythrocyte of UC patients (24.38 ± 11.00, 415.0 ± 87.6, 10.86 ± 4.37 μmol/l, respectively) compared to controls (69.25 ± 21.00, 535.5 ± 69.1, 16.67 ± 3.34 μmol/l, respectively). After 6-month isothiocyanate treatment, the Cu (0.551 ± 0.380 μmol/l), Fe (534.6 ± 23.1 μmol/l), Mg (63.41 ± 11.19 μmol/l) and P (1,089.0 ± 104.2 μmol/l) content in erythrocyte increased significantly. Summarizing the small amount of Raphacol treatment for 6 months alters the element status in moderately active UC. The favorable effect may be connected to the local antioxidant effect of the bioactive agents which may contribute to the increased element absorption.
Malnutrition is a characteristic feature of inflammatory bowel diseases (IBD), often due to unhealthy nutritional habits. Therefore, nutritional habits (intake of vegetables and fruits) and element content in erythrocytes have been investigated. 50 IBD patients (25 male, 25 female) and 50 healthy volunteers (35 male, 15 female) were asked to complete a questionnaire. In addition to routine laboratory parameters, Ca, Cu, Fe, Mg, Mn, P, S and Zn content in erythrocytes were determined w i th ICP-OES. Decreased level of Ca (0.975 ± 0.440 μg/g), Mg (1.02 ± 0.24 μg/g) and Zn (0.776 ± 0.482 μg/g) was observed in IBD patients at P<0.05 level compared to the control (2.90 ± 2.25 μg/g, 18.28 ± 9.66 μg/g and 1.05 ± 0.48 μg/g). IBD patients consume similar foodstuffs to healthy people although in lesser amount. The intake of nutritional antioxidants was almost the same in both groups, whereas element intake differed because of diverse nutritional habits. According to the survey, in Hungary healthy people consume about 18-66% of essential element requirements. In the case of IBD patients the situation is worse (15-60%) because of lesser intake and malabsorption. Lowest element intakes were observed for Ca and Zn. The mineral element imbalance in IBD patients probably contributes to their deficiency. Since IBD patients and the controls are on similar diet, latent element deficiency may develop in healthy volunteers which may enhance the risk of metabolic diseases.
The B-type natriuretic peptide receptor (NPR-B) is a specific receptor for the C-type natriuretic peptide (CNP) and the binding of the peptide to NPR-B stimulates the bone formation by osteoblasts. However, the mechanism behind the regulation of NPR-B expression in osteoblasts remains unknown. In this study, we examined the role of prostaglandin E 2 (PGE 2) through the PGE 2 receptor subtypes, EP1, EP2, EP3 and EP4, in the regulation of NPR-B expression using calvarial osteoblasts from rats of various ages. Reverse Transcription-PCR (RT-PCR) and Western blotting analyses revealed that PGE 2 or 17-phenyl-ω-trinor PGE 2 , an EP1 agonist, increased the expression of NPR-B of calvarial osteoblasts from 25-week-old rats in a time-and dose-dependent manner. The PGE 2 -and EP1 agonist-induced increase in NPR-B expression was blocked by treating with SC19220, an EP1 antagonist. By contrast, agonists for EP2, EP3, and EP4 failed to affect the NPR-B expression. The basal mRNA level of NPR-B and EP1 continuously decreased with the age of cell donors between 10 to 60 weeks and remained constant over 60 weeks. The degree of EP1 agonist-induced increase in NPR-B mRNA level gradually decreased with age of cell donors between 10 to 60 weeks, and no significant effect of EP1 agonist on the NPR-B mRNA level was observed over 60 weeks. From these results, we concluded that PGE 2 acts as a regulator of NPR-B expression through the EP1 receptor in osteoblasts and age-related decrease in EP1 expression causes a decrease in NPR-B expression.
