Qualidade do sono e fatores associados em idosos não-institucionalizados em Rio Verde, Goiás / Sleep quality and associated factors in a group of non-institutionalized elderly people in the city of Rio Verde, Goiás / Calidad del sueño y factores asociados en un grupo de ancianos no institucionalizados de la ciudad de Rio Verde, Goiás

RESUMO Objetivo:avaliar a qualidade do sono e os fatores associados em idosos não-institucionalizados em Rio Verde, Goiás. Método:estudo epidemiológico, transversal e de base populacional, realizado com idosos participantes do projeto da terceira idade, realizado pela Universidade de Rio Verde, entre abril e maio de 2019. A coleta de dados ocorreu com aplicação de três instrumentos, questionário com dados sociodemográficos, questionário de qualidade do sono de Pittsburgh e questionário internacional de atividade física. Para análise dos dados utilizou o teste qui-quadrado. Resultados: foram analisados 73 idosos, dentre os quais 67,1% apresentaram índices ruins de qualidade do sono. Ser do sexo feminino, solteiro ou viúvo, ter baixa escolaridade, não estar aposentado e não usar medicações para dormir apresentou associação significativamente relevante com a má qualidade do sono (p<0,05).Conclusão: grande parte dos idosos apresentaram má qualidade do sono. Isso indica a necessidade decriação de programas e medidas de promoção à saúde ao idoso que incluam rotinas e rituais de sono, técnicas alternativas de relaxamento, prática regular de atividade física, melhorias nas condições ambientais e aspectos sobre a higiene do sono.

ABSTRACTObjective:to evaluate sleep quality and associated factors in non-institutionalized elderly people in Rio Verde, Goiás. Method: epidemiological, cross-sectional, population-based study conducted with elderly participants of the Third Age Project, carried out by the University of Rio Verde, between April and May 2019. Data collection was carried out with the application of three instruments, a questionnaire with sociodemographic data, questionnaire of Pittsburgh sleep quality and the international physical activity questionnaire. For data analysis, the chi-square test was used. Results:73 elderly were analyzed, among which 67.1% had poor sleep quality indices. Being female, single or widowed, having a low level of education, not being retired and not using medications to sleep had a significantly relevant association with poor sleep quality (p<0.05). Conclusion:most of the elderly had poor sleep quality. This indicates the need to create health promotion programs and measures for the elderly that include sleep routines and rituals, alternative relaxation techniques, regular physical activity, improvements in environmental conditions and aspects of sleep hygiene.

RESUMEN Objetivo:evaluar la calidad del sueño y factores asociados en adultos mayores no institucionalizados de la ciudad de Rio Verde, Goiás. Método: estudio epidemiológico, transversal, poblacional realizado con adultos mayores participantes del proyecto tercera edad, realizado por la Universidad de Río Verde, entre abril y mayo de 2019. La recolección de datos se realizó con la aplicación de tres instrumentos, un cuestionario con datos sociodemográficos, cuestionario de calidad del sueño de Pittsburgh y cuestionario internacional de actividad física. Para el análisis de los datos se utilizaron la prueba de chi-cuadrado. Resultados:analizaron 73 adultos mayores, de los cuales el 67,1% presentaba índices de mala calidad del sueño. Ser mujer, soltera o viuda, tener un bajo nivel educativo, no estar jubilado y no usar medicamentos para dormir tuvo una asociación significativamente relevante con la mala calidad del sueño (p <0,05). Conclusión:la mayoría de los adultos mayores tenían mala calidad del sueño. Esto indica la necesidad de crear programas y medidas de promoción de la salud para las personas mayores que incluyan rutinas y rituales del sueño, técnicas alternativas de relajación, actividad física regular, mejoras en las condiciones ambientales y aspectos de la higiene del sueño.

Neuroprotective Effect of 3-[(4-Chlorophenyl)selanyl]-1-methyl-1H-indole on Hydrogen Peroxide-Induced Oxidative Stress in SH-SY5Y Cells.

Extensive data have reported the involvement of oxidative stress in the pathogenesis of neuropsychiatric disorders, prompting the pursuit of antioxidant molecules that could become adjuvant pharmacological agents for the management of oxidative stress-associated disorders. The 3-[(4-chlorophenyl)selanyl]-1-methyl-1H-indole (CMI) has been reported as an antioxidant and immunomodulatory compound that improves depression-like behavior and cognitive impairment in mice. However, the exact effect of CMI on specific brain cells is yet to be studied. In this context, the present study aimed to evaluate the antioxidant activity of CMI in H2O2-induced oxidative stress on human dopaminergic neuroblastoma cells (SH-SY5Y) and to shed some light into its possible mechanism of action. Our results demonstrated that the treatment of SH-SY5Y cells with 4 µM CMI protected them against H2O2 (343 µM)-induced oxidative stress. Specifically, CMI prevented the increased number of reactive oxygen species (ROS)-positive cells induced by H2O2 exposure. Furthermore, CMI treatment increased the levels of reduced glutathione in SH-SY5Y cells. Molecular docking studies demonstrated that CMI might interact with enzymes involved in glutathione metabolism (i.e., glutathione peroxidase and glutathione reductase) and H2O2 scavenging (i.e., catalase). In silico pharmacokinetics analysis predicted that CMI might be well absorbed, metabolized, and excreted, and able to cross the blood-brain barrier. Also, CMI was not considered toxic overall. Taken together, our results suggest that CMI protects dopaminergic neurons from H2O2-induced stress by lowering ROS levels and boosting the glutathione system. These results will facilitate the clinical application of CMI to treat nervous system diseases associated with oxidative stress.

Anhedonic- and anxiogenic-like behaviors and neurochemical alterations are abolished by a single administration of a selenium-containing compound in chronically stressed mice.

Despite the severity and the high prevalence of depression and anxiety and the efforts that have been done to improve their treatment, the available pharmacotherapy still has several limitations. Therefore, the investigation of novel agents and the characterization of the molecular signaling pathways underlying their effects are needed. The organoselenium compound 3-[(4-chlorophenyl)selanyl]-1-methyl-1H-indole (CMI) has emerged as a promising antidepressant and anxiolytic molecule in several animal models of depression through the modulation of neuroinflammation and oxidative stress. In light of this, the present study aimed to dive into the mechanism of action of CMI in ameliorating anhedonic- and anxiogenic-like behaviors induced by repeated corticosterone administration in mice. A single administration of CMI (1 â€‹mg/kg, i.g.) abrogated the behavioral alterations induced by corticosterone in the open field test, splash test, and elevated plus maze test. Additionally, CMI treatment decreased the levels of reactive species and lipid peroxidation in the plasma of corticosterone-treated mice and normalized the expression of GR, BDNF, synaptophysin, GSK-3ß, Nrf 2 , and IDO in the hippocampi of stressed mice. Noteworthy, the pre-treatment of mice with LY294002 (PI3K inhibitor) and rapamycin (mTOR inhibitor) abrogated the anti-anhedonic- and anxiolytic-like effects elicited by CMI in corticosterone-treated mice, while ZnPP (HO-1 inhibitor) counteracted the anxiolytic-like effect of CMI. These findings suggest that CMI might ameliorate behavioral and biochemical alterations in the depression-anxiety comorbidity induced by corticosterone, highlighting the potential of CMI as a possible adjuvant therapy.

Short-term effects induced by nicotinamide in ovariectomized females.

Nicotinamide adenine dinucleotide (NAD)+ precursors such as nicotinamide activate sirtuins and enhance energy metabolism. The aim of this study was to evaluate the metabolic effects of nicotinamide in ovariectomized (OVX) female rats to establish molecular targets against obesity, which support the safe therapeutic application of nicotinamide. The OVX animals were divided into groups: SHAM (simulated surgery), SHAMn (two weeks of 35 mg·kg-1 nicotinamide per day, by gavage), OVX, and OVXn (two weeks of 35 mg·kg-1 nicotinamide per day, by gavage). The results indicated that nicotinamide favored lipolysis, as evidenced by an increase in free fatty acid and hepatic triglyceride levels, which were not fully normalized during the treatment period. The lipolysis appeared to be due to increased SIRT1 and mitochondrial oxidative phosphorylation in muscle and adipose tissue. There were decreases in muscle and fat nicotinamide N-methyltransferase (NNMT), which were associated with decreases in mass and triglyceride, low-density lipoprotein cholesterol (LDLc), and total cholesterol content. Nicotinamide appeared to be beneficial for the glycemic profile, with normal hepatic glycogen storage and a tendency towards insulin sensitivity in the OVXn. In the SHAMn group, nicotinamide led to glucose intolerance, together with reduced muscle expressions of nicotinamide phosphoribosyltransferase (NAMPT) and SIRT3, suggesting that there were no short-term benefits. Supplementation with nicotinamide led to tissue-specific adaptive lipid and molecular changes in OVX rats.

The antioxidant and immunomodulatory compound 3-[(4-chlorophenyl)selanyl]-1-methyl-1H-indole attenuates depression-like behavior and cognitive impairment developed in a mouse model of breast tumor.

Psychiatric alterations are often found in patients with breast cancer even before the initiation of adjuvant therapy, resulting in a poor quality of life. It has become accepted that neuroinflammation and oxidative stress are involved in the pathophysiology of depression and cognitive impairment. Herein, we tested the hypothesis that treatment with the antioxidant and immunomodulatory selenium-containing compound 3-[(4-chlorophenyl)selanyl]-1-methyl-1H-indole (CMI)could attenuate behavioral and neurochemical alterations in a mammary (4T1) tumor model. Female BALB/c mice were subcutaneously inoculated with 4T1 cancer cells (1 × 105 cells/mice) or PBS. From days 14 to 20, mice received daily gavage with canola oil or CMI. On day 21, mice were submitted to behavioral tests followed by euthanasia. We found that CMI did not alter tumor growth, body weight, and body temperature in tumor-bearing mice. Importantly, treatment with CMI abrogated tumor-induced depression-like behavior and cognitive impairment. By the time CMI improved the behavioral alterations, it had reduced tumor-induced neuroinflammation (altered expression of NFκB, IL-1ß, TNF-α, IL-10, IDO, and COX-2) and oxidative stress (altered expression of iNOS and Nrf2, and levels of reactive species, nitric oxide, lipid peroxidation, and superoxide dismutase activity) in the prefrontal cortices and hippocampi of mice. A molecular docking approach suggested the ability of CMI to inhibit the activity of iNOS and COX-2. Together, our results indicate that CMI treatment may attenuate depression and cognitive impairment in 4T1 tumor-bearing mice, and be a groundbreaking strategy for the treatment of cancer-related psychiatric symptoms to improve the quality of life of cancer patients.

Depression-like behavior, hyperglycemia, oxidative stress, and neuroinflammation presented in diabetic mice are reversed by the administration of 1-methyl-3-(phenylselanyl)-1H-indole.

Oxidative stress and neuroinflammation are found both in diabetes mellitus and major depressive disorder (MDD). In addition to damage in peripheral organs, such as liver and kidney, diabetic patients have a higher risk of developing depression. In this sense, the objective of the present study was to characterize the antidepressant-like effect of a selenium-containing compound, the 1-methyl-3-(phenylselanyl)-1H-indole (MFSeI), in streptozotocin (STZ)-induced diabetic mice. STZ (200 mg/kg, i.p.) was used to induce diabetes mellitus type I, and after seven days, the administration of MFSeI (10 mg/kg, i.g.) was initiated and followed for the next 14 days. Twenty-four hours after the last administration of MFSeI, the behavioral tests were performed, followed by euthanasia. The treatment with MFSeI was able to reverse the hyperglycemia induced by STZ. MFSeI also decreased the plasma levels of biomarkers of liver and kidney damage. Importantly, MFSeI reversed the depression-like behavior induced by STZ in the tail suspension test and forced swimming test without promoting locomotor alterations. Furthermore, MFSeI reversed the increased levels of reactive species and lipid peroxidation in the prefrontal cortex (PFC), hippocampus (HC), liver, and kidney of STZ-treated mice. Treatment with MFSeI also decreased the expression of tumor necrosis factor-alpha, inducible nitric oxide synthase and indoleamine 2,3-dioxygenase, while increasing the expression of interleukin-10, insulin receptor substrate-1 and glucose transport-4 in the PFC and HC of mice. Taken together, the results indicate the effectiveness of MFSeI against depression-like behavior and central and peripheral complications caused by diabetes in mice.

Repeated administration of a selenium-containing indolyl compound attenuates behavioural alterations by streptozotocin through modulation of oxidative stress in mice.

Although the pathophysiology of major depression disorder (MDD) is still poorly understood, mounting evidence suggests that the brains of depressed patients are under oxidative stress, leading to depressive symptoms that may include anxiety and cognitive impairment. This study aimed to investigate if the seleno-organic compound 1-methyl-3-(phenylselanyl)-1H-indole (MFSeI) reverses the depression- and anxiogenic-like behaviour, cognitive impairment and oxidative stress induced by the intra-cerebroventricular injection of streptozotocin (STZ; 0.2 mg/4 µl/per mouse) in Swiss male mice. Twenty-four hours after the STZ injection, mice were treated with MFSeI (10 mg/kg, intra-gastrically), or vehicle solution, once daily for seven days. The behavioural tests were performed 30 min after the final MFSeI administration, followed by euthanasia and collection of the cerebral cortex and hippocampus. Administration of MFSeI reversed the depression- and anxiogenic-like behaviour and cognitive impairment induced by STZ, in mice. Neurochemical analyses demonstrated that MFSeI reversed the STZ-increased levels of reactive species, nitrite, lipid peroxidation and acetylcholinesterase activity in the cerebral cortex and hippocampus of mice. Moreover, a single administration of MFSeI (300 mg/kg, intra-gastrically) did not cause acute toxicity in Swiss male mice. Altogether, our data suggest that MFSeI exhibits antidepressant- and anxiolytic-like effects and improves the cognition of STZ-treated mice, without any toxicity.

3-(4-Chlorophenylselanyl)-1-methyl-1H-indole promotes recovery of neuropathic pain and depressive-like behavior induced by partial constriction of the sciatic nerve in mice.

3-(4-Chlorophenylselanyl)-1-methyl-1H-indole (CMI) is an organoselenium compound that presents antioxidant activity, antinociceptive, anti-inflammatory and antidepressive-like effect in mice in previous studies conducted by our research group. In this study, we evaluate the anti-allodynic, anti-hyperalgesic and antidepressant-like effects of CMI on partial sciatic nerve ligation (PSNL) in male adult Swiss mice (25-35 g) as well as the involvement of oxidative stress in these effects. Mice underwent PSNL surgery and after 4 weeks they were treated with CMI (10 mg/kg, intragastric route [i.g.]) or vehicle. The treatment with CMI (10 mg/kg, i.g.) reversed the increased the percentage of response to Von-Frey Hair (VFH) stimulation, decreased the latency time to nociceptive response in the hot-plate test, increased immobility time in the forced swimming test (FST) and decreased groomings activity in the splash test, all induced by PSNL. Additionally, CMI also reversed increased the levels of reactive oxygen species (ROS) and lipid peroxidation in cortex and hippocampus and plasmatic levels of corticosterone in mice, induced by PSNL. Results demonstrate that CMI reversed behavioral and biochemical alterations in the dyad pain-depression induced by PSNL and possibly modulation of oxidative system.

Effects of a selanylimidazopyridine on the acute restraint stress-induced depressive- and anxiety-like behaviors and biological changes in mice.

In the last decades, selenium-containing compounds have received increasing attention due to their various biological and pharmacological properties. In the present study, we investigated the effects of 3-[(4-methoxyphenyl) selanyl]-2-phenylimidazo[1,2-a] pyridine (MPI; 1, 10 or 50 mg/kg, i.g.) on the acute restraint stress (ARS)-induced depressive- and anxiety-like behaviors in mice and its underlying mechanism of action. We used the open filed test, forced swimming test, and splash test to evaluate depressive-like behavior, and marble burying and elevated plus maze test to measure anxiety-like behavior. We found that MPI attenuated ARS-induced depressive- and anxiety-like behaviors in all behavioral tests, without having an effect in non-stressed mice. MPI prevented the increased in pro-inflammatory cytokines, indoleamine-2,3-dioxygenase (IDO) and inducible nitric oxide synthase (iNOS) expression in brain structures via canonical nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) down-regulation. Additionally, MPI prevented ARS-induced downregulation of brain-derived neurotrophic factor (BDNF), increased reactive oxygen/nitrogen species generation and lipid peroxidation in prefrontal cortex and hippocampus of mice. In addition, MPI blocked the downregulation of glucocorticoid receptors in the prefrontal cortex and hippocampus and reduced the increased circulating level of corticosterone in stressed mice. These results suggested that MPI showed antidepressant- and anxiolytic-like properties and the effects might be associated with the biological changes in the prefrontal cortex and hippocampus.

Antidepressant-like effect of a new selenium-containing compound is accompanied by a reduction of neuroinflammation and oxidative stress in lipopolysaccharide-challenged mice.

Organoselenium compounds and indoles have gained attention due to their wide range of pharmacological properties. Depression is a recurrent and disabling psychiatric illness and current evidences support that oxidative stress and neuroinflammation are mechanisms underlying the pathophysiology of this psychiatric condition. Here, we evaluated the effect of 3-((4-chlorophenyl)selanyl)-1-methyl-1H-indole (CMI) in lipopolysaccharide (LPS)-induced depressive-like behaviour, neuroinflammation and oxidative stress in male mice. CMI pre-treatment (20 and 50 mg/kg, intragastrically) significantly attenuated LPS (0.83 mg/kg, intraperitoneally)-induced depressive-like behaviour in mice by reducing the immobility time in the tail suspension test (TST) and forced swimming test (FST). CMI pre-treatment ameliorated LPS-induced neuroinflammation by reducing the levels of interleukin (IL)-1ß, IL-4 and IL-6 in the hippocampus and prefrontal cortex, as well as markers of oxidative damage. Additionally, we investigated the toxicological effects of CMI (200 mg/kg, i.g.) in the liver, kidney and brain through determination of the activity of aspartate aminotransferase (AST), alanine aminotransferase (ALT), δ-aminolevulinate dehydratase (δ-ALA-D) and creatinine levels. These biomarkers were not modified, indicating the possible absence of neuro-, hepato- and nephrotoxic effects. Our results suggest that CMI could be a therapeutic approach for the treatment of depression and other neuropsychiatric disorders associated with inflammation and oxidative stress.

Low-level laser therapy reduces delayed hypersensitivity reaction to ovalbumin in Balb/C mice.

The aim of this study was to evaluate the effect of low-level laser therapy (LLLT) in an experimental model of delayed hypersensitivity reaction (DTH). LLLT has been used clinically to treat numerous diseases and has been tested in different experimental models, but some of its effects have yet to be explained. We assessed the effects of LLLT on DTH to ovalbumin (OVA), a protein that has commonly been used as an antigen to sensitize laboratory animals. This experimental model is broadly used to assess the effects of substances that can potentially modulate the immune system and inflammatory reactions. Balb/C mice were randomly divided into four groups: (I) immunized, untreated, and challenged (n = 6); (II) not immunized, untreated, and challenged (n = 6); (III) immunized, treated with azathioprine (AZA), and challenged (n = 6); and (IV) immunized, treated with LLLT, and challenged (n = 6). Forty-eight hours after the challenge, the animals were submitted to a paw edema test and euthanized for histopathology analysis of their plantar pads. The results obtained in DTH units were as follows: Group I, 19.6 ± 8.9; Group II, 5.8 ± 2.6; Group III, 5.6 ± 2.5; and Group IV, 5.2 ± 2.6. DTH was less intense for the groups treated with AZA and laser compared with Group I (p < 0.05). We observed no statistical difference between the AZA- and LLLT-treated groups. The slides obtained from the footpad specimens showed that AZA and laser acted similarly on the normal pattern of DTH triggering. Our results suggest that treatment with LLLT has an immunomodulatory effect on DTH to OVA.

Low-level laser therapy increases transforming growth factor-beta2 expression and induces apoptosis of epithelial cells during the tissue repair process.

BACKGROUND DATA: Low-level laser therapy (LLLT) has been reported to modulate the healing of wounds by inducing an increase in mitotic activity, fibroblast number, synthesis of collagen, and neovascularization. OBJECTIVE: In the present study we evaluated the effect of LLLT on expression of TGF-beta(2), an immunosuppressive cytokine, at the site of tissue repair, using an experimental rat model to study cutaneous wound healing. In addition, we also investigated the presence of apoptotic cells in epithelial and connective tissue. MATERIALS AND METHODS: Thirty male Wistar rats were divided into two groups: group 1, which was subjected to surgical skin wounds only (n = 15), and group 2, which was subjected to surgical skin wounds followed by LLLT (n = 15). In group 2, the LLLT was given with these parameters: 15 mW of power, a dose of 3.8 J/cm(2), for 15 sec for three applications. At 10 d post-surgery and laser application the animals were sacrificed with an overdose of anesthetic and tissue samples from the wounds were submitted to immunohistochemistry and in-situ detection of apoptosis. RESULTS: Most of the inflammatory cells and fibroblasts were TGF-beta(2)-positive, and many apoptotic epithelial cells and fibroblasts were seen in the tissue samples from the LLLT-treated animals. However, a few apoptotic epithelial cells and fibroblasts were also seen in the samples obtained from control animals. CONCLUSION: Our results indicate that LLLT may be an important inducer of apoptosis during the process of tissue repair. In addition, we demonstrated that LLTT has an immunomodulatory effect on TGF-beta(2) expression at sites of wound healing.

Effects of low-level laser therapy on the progress of wound healing in humans: the contribution of in vitro and in vivo experimental studies: [review]

Low-level laser therapy is an important method for the treatment of healing processes, and several experimental studies have been carried out in search of a greater understanding of its therapeutic possibilities. The objective of this study was to review pathogenetic aspects of soft tissue repair to better understand skin lesion healing and the role of low-intensity laser in the progression of tissue healing. This study consists of a concise review of scientific literature data on the use of low-level laser and its influence on wound healing. Many studies have extensively covered the effects of using laser radiation in tissues, describing its beneficial aspects in tissue healing. However, many unanswered questions demand research on the mechanism of action and on parameters of low-level laser use in different stages of wound repair to clarify how this method acts at a cell level in healing processes.