RESUMO
In recent years there have been an increasing number of in vitro and in vivo studies that show positive results regarding antimicrobial photodynamic therapy (aPDT) used in dentistry. These include applications in periodontics, endodontics, and mucosal infections caused by bacteria present as biofilms. Antimicrobial photodynamic therapy is a therapy based on the combination of a non-toxic photosensitizer (PS) and appropriate wavelength visible light, which in the presence of oxygen is activated to produce reactive oxygen species (ROS). ROS induce a series of photochemical and biological events that cause irreversible damage leading to the death of microorganisms. Many light-absorbing dyes have been mentioned as potential PS for aPDT and different wavelengths have been tested. However, there is no consensus on a standard protocol yet. Thus, the goal of this review was to summarize the results of research on aPDT in dentistry using the PubMed database focusing on recent studies of the effectiveness aPDT in decreasing microorganisms and microbial biofilms, and also to describe aPDT effects, mechanisms of action and applications.
RESUMO
The purpose of this study was to determine whether the aerobic training-induced fiber-type transition in different muscles is associated with alterations in NFAT isoforms gene expression. We hypothesized that the aerobic training-induced fiber-type transition would be mediated by NFATc1-c3 isoforms without altering the CaN expression. Male Wistar rats (80 days old) were divided into a trained group (T; n=8) that underwent an 8-wk swimming endurance training program (5 days/week) and a control group (C; n=8). After the experimental period, the animals were sacrificed, and the soleus (SOL) and plantaris (PL) muscles were collected for morphometrical, histochemical and molecular analyses. Aerobic training induced a type I-to-type IIA fiber transition in the SOL muscle and a type IIB-to-type IIA fiber transition in the PL muscle, which were concomitant with a significant (p<0.05) increase in NFATc1-c3 gene expression in both the SOL and PL muscles. In contrast, the expression levels of calcineurin (CaN) and NFATc4 remained unchanged. Therefore, our results showed that fiber type switching induced by aerobic training is mediated by NFATc1-c3 isoforms without altering the CaN expression.
Assuntos
Calcineurina/metabolismo , Fibras Musculares de Contração Rápida/metabolismo , Fibras Musculares de Contração Lenta/metabolismo , Fatores de Transcrição NFATC/metabolismo , Natação/fisiologia , Animais , Biomarcadores/metabolismo , Masculino , Cadeias Pesadas de Miosina/metabolismo , Resistência Física/fisiologia , Isoformas de Proteínas/metabolismo , Distribuição Aleatória , Ratos , Ratos Wistar , Reação em Cadeia da Polimerase em Tempo Real , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Fatores de Transcrição/metabolismoRESUMO
The involvement of nitric oxide (NO) in anxiety was investigated in rats, using the elevated plus maze test. Acute, but not chronic, systemic treatment with N omega-nitro-L-arginine methyl ester (L-NAME, 10 and 60 mg.kg-1), an inhibitor of NO synthase, increased the time spent by the rats in the open arms. Both the acute and chronic treatments with L-NAME inhibited NO synthase in endothelial cells and in the central nervous system, as shown by the increase in mean arterial pressure and decreased NO synthase activity in brain tissue. Chronic treatment with L-NAME also decreased the serum nitrate levels. The anxiolysis induced by acute L-NAME treatment is unlikely to be due to hypertension, since two-kidney one-clip hypertension in non-L-NAME-treated rats failed to significantly change exploratory behaviour in the elevated plus maze. These results indicate that acute inhibition of NO synthesis decreases anxiety in rats.
Assuntos
Ansiedade/tratamento farmacológico , Inibidores Enzimáticos/uso terapêutico , Aprendizagem em Labirinto/efeitos dos fármacos , NG-Nitroarginina Metil Éster/uso terapêutico , Óxido Nítrico Sintase/antagonistas & inibidores , Análise de Variância , Animais , Ansiolíticos/farmacologia , Ansiolíticos/uso terapêutico , Ansiedade/fisiopatologia , Arginina/farmacologia , Arginina/uso terapêutico , Pressão Sanguínea/efeitos dos fármacos , Encéfalo/efeitos dos fármacos , Encéfalo/enzimologia , Sistema Nervoso Central/efeitos dos fármacos , Diazepam/farmacologia , Diazepam/uso terapêutico , Inibidores Enzimáticos/administração & dosagem , Inibidores Enzimáticos/farmacologia , Hipertensão Renal/induzido quimicamente , Hipertensão Renal/fisiopatologia , Masculino , NG-Nitroarginina Metil Éster/administração & dosagem , NG-Nitroarginina Metil Éster/farmacologia , Nitratos/sangue , Óxido Nítrico/metabolismo , Óxido Nítrico/fisiologia , Ratos , Ratos WistarRESUMO
AIMS: Since patients who regularly take NSAIDS may use sucralfate because of its cytoprotective properties, we examined the influence of this compound on the pharmacokinetics of diclofenac. METHODS: Potassium diclofenac (105 mg) was administered orally to eighteen healthy male volunteers with or without a 5-day pre-treatment with sucralfate (2000 mg twice daily). Blood samples were collected at intervals post-dose and serum concentrations of diclofenac were determined by reverse-phase h.p.l.c. RESULTS: Pre-treatment with sucralfate significantly decreased both the AUC(0,8 h) [2265 ng h ml-1 (geometric mean) (range 1815-2827) vs 1821 ng h ml-1 (1295-2562)] and the Cmax [1135 ng ml-1 (geometric mean) (range 898-1436) 701 ng ml-1 (501-981)] with no significant delay in absorption [tmax 1.0 h (median) (range 0.5-2.0) vs 1.0 h (0.5-4.0)]. CONCLUSIONS: The short-term treatment of healthy male volunteers with sucralfate decreases potassium diclofenac bioavailability. These findings suggest that either an appropriate increase in the diclofenac intake or the use of another gastric mucosa protector must be adopted.
Assuntos
Anti-Inflamatórios não Esteroides/farmacocinética , Diclofenaco/farmacocinética , Fármacos Gastrointestinais/farmacologia , Sucralfato/farmacologia , Absorção/efeitos dos fármacos , Administração Oral , Adulto , Estudos Cross-Over , Humanos , Modelos Lineares , MasculinoRESUMO
BACKGROUND: An oral triple therapy using sucralfate instead of a bismuth to eradicate Helicobacter pylori has yielded worse results than those obtained with conventional oral triple therapies. To date, the effect of sucralfate on the pharmacokinetics of nitroimidazolic compounds used in triple therapy such as with metronidazole is unknown. The aim of this study was to investigate the effect of a 5-day administration period of sucralfate (2 g b.i.d.) on metronidazole pharmacokinetics. METHODS: Fourteen healthy male volunteers were selected. The study had an open randomized 2-period crossover design with a 14-day washout period between the phases. The plasma concentration of metronidazole and its hydroxy-metabolite were measured by reverse-phase HPLC with ultraviolet detection. RESULTS: No statistically significant difference was observed in any of the pharmacokinetic parameters studied in the absence and presence of sucralfate. CONCLUSION: Our results clearly indicate that short-term treatment with sucralfate in healthy volunteers does not alter the extent or the rate of metronidazole absorption, and does not affect metronidazole clearance.
Assuntos
Antiulcerosos/farmacologia , Antitricômonas/farmacocinética , Metronidazol/farmacocinética , Sucralfato/farmacologia , Absorção , Administração Oral , Adulto , Antiulcerosos/administração & dosagem , Antitricômonas/administração & dosagem , Antitricômonas/sangue , Cromatografia Líquida de Alta Pressão , Estudos Cross-Over , Relação Dose-Resposta a Droga , Interações Medicamentosas , Helicobacter pylori/efeitos dos fármacos , Helicobacter pylori/metabolismo , Humanos , Absorção Intestinal/efeitos dos fármacos , Masculino , Metronidazol/administração & dosagem , Metronidazol/sangue , Sucralfato/administração & dosagemRESUMO
The bioavailability of a single dose of a potassium diclofenac (KDIC) suspension (Flogan, Merck, 7ml, 105 mg) was studied in 13 healthy male volunteers in the fasting state (placebo phase, PLA), after gastric acid secretion blockade (subacute pretreatment with omeprazole, OME phase) and after food intake (FOOD phase). A 14-day washout period between phases was adopted. Serum samples were obtained over a 24 hour interval and the diclofenac concentrations were determined by high pressure liquid chromatography with ultraviolet detection. From the serum diclofenac concentration vs time curves, the AUC[0-infinity] (area under the concentration vs time curves from 0 to infinity), Cmax (maximum achieved concentration), tmax (time to achieve Cmax), Ke (terminal first order elimination constant), half-life values (t1/2) and AUC[0-infinity]/t1/2 ratio as an index of diclofenac clearance, were obtained. All these variables were analyzed using both parametric and non-parametric statistics. In the presence of food, KDIC absorption was delayed (as shown by lower Cmax and greater tmax values) and decreased (as shown by lower AUC[0-infinity] values), and the serum diclofenac concentration vs time curves showed a biphasic pattern. Omeprazole pretreatment did not change the absorption parameters. Both of these treatments altered the diclofenac clearance, as assessed by the AUC[0-infinity]/t1/2, t1/2 and Ke values, although the changes were not considered to be clinically significant, because of the wide therapeutic range for diclofenac. The delay in the rate of diclofenac absorption produced by food intake was not due to an increase in the gastric pH, and could be of particular importance when rapid analgesia is desired.