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1.
J Sleep Res ; 31(6): e13700, 2022 12.
Artículo en Inglés | MEDLINE | ID: mdl-35896519

RESUMEN

Older adults with poor sleep tend to show a discrepancy between objective and self-reported sleep parameters, which can trigger a vicious cycle that worsens their sleep complaints. Cognitive-behavioural therapy can reduce this discrepancy, but alternative behavioural therapies remain untested. The present exploratory study aimed to investigate the effects of mindfulness-based therapy for insomnia (MBTI) on reducing sleep discrepancies in comparison with a sleep hygiene, education, and exercise programme (SHEEP). Older adults were randomly allocated into the mindfulness-based therapy for insomnia group (n = 55) or the sleep hygiene, education, and exercise programme group (n = 58). Subjective and objective sleep parameters were measured using sleep diaries, polysomnography (PSG), and actigraphy. Sleep discrepancies were calculated using the Bland-Altman method for sleep onset latency (SOL) and wake after sleep onset (WASO). Additionally, correlations between the change in sleep discrepancies and the change in subjective sleep quality and trait mindfulness were measured within each group. Sleep onset latency discrepancy measured by polysomnography and actigraphy decreased significantly after the MBTI and SHEEP interventions. In contrast, there was no significant change in wake after sleep onset discrepancy in either group. The change in sleep onset latency discrepancy was correlated with the change in insomnia symptoms and objectively measured trait mindfulness. Mindfulness-based therapy for insomnia was effective in reducing sleep onset latency discrepancies and improving sleep perception in older adults with sleep disturbances, which in turn drove an improvement in sleep quality and insomnia symptoms. Increases in trait mindfulness may have been an important mechanism in improving sleep perception in the mindfulness-based therapy for insomnia group.


Asunto(s)
Atención Plena , Trastornos del Inicio y del Mantenimiento del Sueño , Humanos , Trastornos del Inicio y del Mantenimiento del Sueño/terapia , Higiene del Sueño , Sueño , Actigrafía/métodos , Terapia por Ejercicio
2.
Biomed Res Int ; 2019: 5815604, 2019.
Artículo en Inglés | MEDLINE | ID: mdl-31380432

RESUMEN

BACKGROUND: Sasa quelpaertensis Nakai extract (SQE) or dwarf bamboo has been extensively investigated for its antioxidant and anti-inflammatory effects; however, no previous study assessed its effect as an antidepressant agent. Therefore, this study was designed to examine the effect of oral SQE administration in ameliorating menopausal depressive symptoms and to evaluate its mechanisms in ovariectomized rats with repeated stress. METHODS: All experimental groups except normal group underwent ovariectomy and then immobilization for 14 consecutive days. During these 2 weeks, two rat groups received SQE (100 and 300 mg/kg orally) and their cutaneous body temperature was measured. The tail suspension test (TST) and forced swim test (FST) were performed in order to evaluate depression-like behavior. Additionally, enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry were carried out to evaluate the central monoaminergic neurotransmitter levels and activity. RESULTS: Oral SQE (100 mg/kg) administration had reduced immobility time in TST and FST. Additionally, the SQE 100 and 300 mg/kg administration had decreased the cutaneous body temperature in the rats compared to those without treatment. In ELISA analysis, the SQE 100 group expressed elevated levels of serotonin and dopamine in the hypothalamus, prefrontal cortex, and hippocampus. Antityrosine hydroxylase (anti-TH) antibodies showed a tremendous increase in the density of TH positive cells in the locus coeruleus (LC) region of the SQE 100 group. Likewise, the SQE 100 elevated the number of tryptophan hydroxylase (TPH) and protein kinase C (PKC) immunoreactive cell counts and density in the hypothalamic region. CONCLUSION: These results suggested that the oral SQE administration induced the antidepressant-like effect in the ovariectomized rats with repeated stress via upregulating the levels of serotonin and dopamine through enhancing the expression of TH, TPH, and PKC in many brain areas.


Asunto(s)
Antidepresivos/química , Depresión/tratamiento farmacológico , Extractos Vegetales/química , Sasa/química , Animales , Antidepresivos/farmacología , Modelos Animales de Enfermedad , Ensayo de Inmunoadsorción Enzimática , Suspensión Trasera/métodos , Humanos , Ovariectomía , Extractos Vegetales/farmacología , Hojas de la Planta/química , Ratas , Natación
3.
Biomedicines ; 6(4)2018 Nov 21.
Artículo en Inglés | MEDLINE | ID: mdl-30469388

RESUMEN

BACKGROUND: This study aimed to investigate the antidepressant-like effect of lactate and elucidate its mechanisms in ovariectomized rats with repeated stress. METHODS: Two experiments were conducted on female rats in which all groups, except normal, were ovariectomized and underwent immobilization for 14 days. Lactate was administered orally (100, 250, and 500 mg/kg) for 14 consecutive days, and the rats' cutaneous body temperature was measured during the same period. Depression-like behavior in rats was assessed by the tail suspension test (TST) and forced swimming test (FST). Furthermore, enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry were conducted to evaluate the changes that occurred in the neurotransmitter levels and activity. RESULTS: The lactate 100 and 250 groups had reduced time spent immobile in TST and FST and decreased peripheral body temperature. In ELISA tests, the lactate 250 group expressed elevated levels of serotonin and dopamine in many brain areas. Tyrosine hydroxylase (TH), tryptophan hydroxylase (TPH), and protein kinase C (PKC) immunoreactive cells showed increased density and cell counts in lactate administered groups. CONCLUSION: Results indicated that lactate has an antidepressant effect that is achieved by activation of PKC and upregulation of TH and TPH expression, which eventually leads to enhanced serotonin and dopamine levels in the menopausal rat's brain.

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